Comprehensive Physiology Wiley Online Library

Pulmonary Circulation

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Pulmonary Hemodynamics
1.1 Pulmonary Blood Flow: General Aspects
1.2 Pulmonary Blood Flow and Pressure Waves
1.3 Mechanical Influences on Pulmonary Blood Flow
1.4 Pulmonary Vascular Pressures
1.5 Pulmonary Blood Volume
1.6 Pressure‐ Volume, Pressure‐Flow Relationships
2 Vasomotor Regulation
2.1 Level of Initial Tone
2.2 Detection of a Vasomotor Response
2.3 Sites of Pulmonary Vasoconstriction
2.4 Vasomotor Mechanisms
3 Bronchial Circulation
3.1 Determination of Bronchial Blood Flow
3.2 Normal Levels of Bronchial Blood Flow
3.3 Bronchial Circulation in the Normal Lung
3.4 Bronchial Circulation in Disease
4 Fetal and Neonatal Pulmonary Circulation
4.1 Morphologic Changes
4.2 Regulation of Fetal Pulmonary Circulation
4.3 Postnatal Pulmonary Vasodilation
5 Pulmonary Hypertension
5.1 Pathogenesis
5.2 Experimental Chronic Pulmonary Hypertension
5.3 Pulmonary Vasodilators
5.4 Endothelium‐Dependent Pulmonary Vasodilation
Figure 1. Figure 1.

gRenin‐angiotensin system. The lungs play a central role in control of systemic blood pressure because of the converting enzyme on the luminal aspect of pulmonary capillary endothelium. Strategic disposition of the enzyme and huge expanse of pulmonary capillary endothelium enable rapid and efficient conversion of angiotensin I to angiotensin II as blood courses through the lungs.

Figure 2. Figure 2.

Muscular pulmonary arteries (resistance vessels) in pulmonary circulation of various animal species. Elastic Van Gieson's stain. A: dog; × 500. B: cat; × 500. C: human; × 200. D: rat; × 800. A‐D: tunica media is relatively thin. E: guinea pig; × 200. Tunica media consists of crescentic masses of circular smooth muscle disposed in discontinuous segments resembling sphincters. In areas between sphincterlike masses of smooth muscle the wall consists only of an elastic lamina. F: cow; × 500. Tunica media is thick.

Micrographs courtesy of J. M. Kay
Figure 3. Figure 3.

Four‐quadrant diagram illustrating respiratory and circulatory adaptation by which O2 requirement is satisfied at rest (inner rectangle) and during exercise (outer rectangle). , concentration of O2 in arterial blood; Cvo2, concentration of O2 in venous blood; CAP area, capillary area; DL, diffusing capacity of the lungs; Hb, hemoglobin; , O2 capacity of hemoglobin; , mean alveolar O2 tension; , mean capillary O2 tension; , arterial O2 saturation; , venous O2 saturation.

Adapted from Barcroft
Figure 4. Figure 4.

Pulsatility in pulmonary circulation of the dog. A: transformation of pressure‐flow pulses along length of pulmonary circulation. Transmission time for pressure pulse from pulmonary artery to capillaries ∼0.09 s; from capillaries to veins, transmission time ∼0.03 s. B: top, changes in pulmonary blood volume of the dog at rest and exercise during a single cardiac cycle. Rate of change in pulmonary blood volume (striped area) equals difference between flows in main pulmonary artery and in pulmonary veins . Bottom, storage as calculated from discharge curves at consecutive sections of pulmonary vascular tree during a cardiac cycle. Spa, storage in pulmonary arteries; Spv, storage in pulmonary veins; ST, total storage. Most storage occurs within the pulmonary arterial tree. [A from Wiener, Fishman, et al. , by permission of the American Heart Association, Inc. B from Skalak, Fishman, et al. .]

Figure 5. Figure 5.

Propagation of pressure pulses (left) and flow pulses (right) through pulmonary circulation. Left: top and bottom curves, measured boundary pressures from which all other pressures and flows in the model were calculated. Dashed curves, sum of the mean pressure plus pressure oscillations propagated from right ventricle (arterial pulse). Solid curves include contribution of oscillatory part of left atrial pressure (venous pulse) and represent total (mean + arterial pulse + venous pulse) pressure at each location. Right: corresponding curves for flow. In contrast to left panel, for which top and bottom curves were determined experimentally, all curves in right panel were computed. Tracings, from top to bottom: main pulmonary artery, segmental pulmonary artery (generation 6), precapillaries, postcapillaries, segmental pulmonary vein (generation 38), and left atrium.

From Wiener, Fishman, et al. , by permission of the American Heart Association, Inc
Figure 6. Figure 6.

Principle of a Starling resistor. Thin‐walled collapsible tube traverses a closed chamber (A) in which pressure can be varied at will. Fluid flows from reservoir (R) into collecting vessel (striped area), traversing collapsible tube en route. When outflow pressure exceeds chamber pressure (left), flow is determined by difference between inflow and outflow pressure. However, when chamber pressure exceeds outflow pressure, so that collapsible tube closes (arrow), flow is determined by difference between inflow and chamber pressure.

Adapted from West et al.
Figure 7. Figure 7.

Zones of the lungs in different body positions as determined by interplay between pulmonary vascular (Ppv) and alveolar pressures (PA). For simplicity, only zones 1, 2, and 3 are shown. Ppa, pulmonary arterial pressure.a

Adapted from Hughes
Figure 8. Figure 8.

Blood flow in upright lung as function of vertical height.

Adapted from Glazier et al.
Figure 9. Figure 9.

Topographical distribution of pulmonary blood flow according to relationship among pulmonary arterial pressure (Ppa), pulmonary venous pressure (Ppv), and alveolar pressure (PA). Because of effect of surface tension, PA is more accurately pericapillary pressure. Zone 1 (apex): PA > Ppa > Ppv. No flow (except through corner vessels) because collapsible vessels close when pericapillary pressure exceeds the pressure inside the vessels. Vessels that close are capillaries and other alveolar vessels up to ∼30 μm diam. Zone 2: Ppa > PA > Ppv. Driving pressure is Ppa — PA. This difference increases down lung and so does flow. Zone 3: Ppa > Ppv > PA. Driving pressure is Ppa — Ppv. Although Ppa — Ppv does not change down lung, Ppa and Ppv continue to increase from top to bottom. Flow down zone 3 is less than zone 2. Zone 4 (appears at residual volume): this region of decreased flow appears during forced exhalation and has been attributed to either an increase in interstitial pressure at lung bases or to closure of small airways at low lung volumes as the increase in PA creates either zone 1 or zone 2 conditions.

Adapted from West et al. and Anthonisen and Milic‐Emili
Figure 10. Figure 10.

Alveolar, corner, and extra‐alveolar vessels. A: large extra‐alveolar artery (A) showing its muscle layer surrounded by a loose connective tissue sheath. Alveolar septa, inserted radially, presumably exert a radial outward pull that is responsible for dilation of these vessels as the lung is inflated. Lung parenchyma is characteristic of zone 2. a, Bundles of capillaries (corner vessels); b, flat septa containing open but smoothened, slitlike capillaries; c, septa containing completely closed (derecruited) capillaries. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. After 2 full inflations, peak arterial pressure = 11–12 mmHg, alveolar pressure = 10 mmHg. Thin epoxy section. B: bundle of wide‐open capillaries (a) within reversible folds of alveolar walls in a corner area. Bundles communicate with vessels (V) larger than capillaries, here probably a small nonmuscular artery that is part of the corner arrangement. Although this vessel cannot expand with inflation, it is also protected against collapse. In other locations, small veins are also visible in this arrangement. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. Thin epoxy section. C: capillaries inside a bundle of capillaries (a) in corner presumably connect small arteries with small veins (cf. B) and are protected against excess alveolar pressure. Arrangement is due to reversible pleating of alveolar walls. Some septal capillaries (b) are open but flattened, whereas others (c) are derecruited. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. Thin epoxy section. D: large extra‐alveolar vein (V) is surrounded by a loose connective tissue sheath. Bottom right, pleural surface. Normal rat lung fixed by instillation of fixatives into trachea after lung collapse. Relatively thick paraffin section, hematoxylin and eosin stain.

Micrographs courtesy of J. Gil
Figure 11. Figure 11.

Cross section of alveolar capillary from human lung lined by endothelium (EN). Endothelial nucleus is striking. Alveolar‐capillary barrier is organized into thick (right) and thin (left) portions. Thick side includes considerable interstitial space (IN), containing connective tissue elements, e.g., fibers (cf). In contrast, interstitial space on thin side is obliterated by fusion of basement membranes, which forms a minimal air‐blood barrier. C, capillary containing 3 red corpuscles in its lumen; EP, alveolar epithelium; F, fibroblast.

From Weibel
Figure 12. Figure 12.

Schematic representation of fascial sheath extending down wall of pulmonary arteriole.

Adapted from Hayek
Figure 13. Figure 13.

Pulmonary vascular pressures in consecutive segments of the pulmonary vascular tree and in comparable segments of a systemic artery. Measurements were made by direct puncture of arterial and venous segments of the subpleural microcirculation.

Adapted from Bhattacharya et al.
Figure 14. Figure 14.

Simultaneous tracings in the dog of pulmonary arterial and venous flow and pulmonary arterial and venous pressure. Variations in pulmonary arterial and venous flow are nearly simultaneous; maxima and minima in venous flow lag from corresponding points in arterial flow record only by the 0.09 s necessary for flow pulse to be propagated across pulmonary circulation.

From Morkin, Fishman, et al.
Figure 15. Figure 15.

Principle of determination of pulmonary wedge pressure. Pressure sensed by wedged catheter (left, balloon inflated) is same as that at conjunction of flowing (2 arrows) and static streams (distal to wedged catheter). Nonocclusive constriction distal to occlusive catheter does not affect determination of pulmonary wedge pressure. However, constriction distal to confluence, as in pulmonary venule (PV), may cause pulmonary wedge pressure to exceed left atrial (LA) pressure.

Adapted from Marini
Figure 16. Figure 16.

Effect of location of tip of wedged catheter on validity as measure of left atrial pressure (Pla); one catheter was wedged high (Pwh) and the other low (Pwl) in the lung. Initially the upper catheter was located in zone 2 of the lung and did not reflect left atrial pressure. Saline infusion increased left atrial pressure and converted lung containing upper wedged catheter to zone 3 conditions; both catheters then reflected left atrial pressures. Subsequent hemorrhage restored zone 2 conditions and original discrepancy between pulmonary wedge and left atrial pressures. Catheter that was wedged low operated throughout under zone 3 conditions.

From Todd et al.
Figure 17. Figure 17.

Effect of exercise on upright lung. Increase in mean pulmonary arterial pressure, coupled with increase in pulsatility, favors apical perfusion.

Adapted from West
Figure 18. Figure 18.

Pulmonary hemodynamics at rest and during steady‐state supine exercise in humans. A: normal males, avg age 23.6 ± 2.1 SD. B: normal females, avg age 23.8 ± 3.9 SD. BA, brachial arterial pressure; C.O., cardiac output; d, diastolic pressure; HR, heart rate; m, mean pressure; PAP, pulmonary arterial pressure; PCW, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; s, systolic pressure.

Adapted from Gurtner et al.
Figure 19. Figure 19.

Passive changes in pulmonary vascular resistance (R) at different levels of driving pressure and pulmonary blood flow (). Pulmonary venous pressure is assumed to remain constant. Pulmonary vascular resistance decreases as either blood flow or pressure drop increases.

Figure 20. Figure 20.

Pulmonary vascular pressure‐flow curves for detection of pulmonary vasomotor activity. A: theoretical basis for detecting pulmonary vasomotor activity with respect to passive pressure‐flow curves in the same individual. Solid line, passive pressure‐flow curve for the individual. Points A and B, linear incremental changes in pressure and flow along passive pressure‐flow curve. Point C, active change in pulmonary vascular resistance. B: practical application of passive pressure‐flow curves to detect vasomotor activity. Left: passive pressure‐flow curve has been established for the individual by measurements at 2 levels of blood flow, i.e., at rest and during exercise (EX). During a single trial of acute hypoxia, point falls above passive pressure‐flow curve, i.e., on a new curve that lies above the passive curve, suggesting that pulmonary vasoconstriction has occurred. Right: similar plot with calculated pulmonary vascular resistance instead of pressure drop as ordinate.

A courtesy of D. Silage
Figure 21. Figure 21.

Use of linear portions of a family of pulmonary vascular resistance curves as isopleths to display effect of test procedure on pulmonary vascular resistance. Right, resistance values (R units). At rest (•), pulmonary vascular resistance is higher at sea level than at altitude. During exercise (→), resistance values decrease in both instances, moving in each case to a lower resistance isopleth.

Figure 22. Figure 22.

Top: input impedance spectrum in main pulmonary artery of normal anesthetized dog. Pattern is similar to that of the ascending aorta but lower in amplitude. Minimal value of impedance modulus and crossover of impedance phase occurs at ∼6–8 Hz. Pulmonary hypertension secondary to valvular heart disease is associated with an increase in pulmonary arterial input impedance and a shift of minimal impedance modulus to right. Bottom: impedance phase. Flow in normal lung leads pressure at lower frequencies (negative phase); situation is reversed at higher frequencies.

Adapted from Milnor
Figure 23. Figure 23.

Arachidonic acid cascade, illustrating 2 pathways and some metabolic products able to change pulmonary vasomotor tone. Metabolic pathways of arachidonic acid initiated by cyclooxygenase and lipoxygenase catalyzed reactions. By stimulating a phospholipase the leukotrienes may in turn cause release of products of cyclooxygenase pathway.

Figure 24. Figure 24.

Putative sites of action of acute hypoxia. Pulmonary microvessel (artery, capillary, and vein) is shown traversing alveolar portion of the lung. Precapillary vessel is subdivided into proximal conducting segment (A), in which mixed venous blood (MVB ) affects some critical element of the vascular smooth muscle, and terminal segment (B), in which alveolar ordinarily is the major influence (striped area). Top: air breathing. Low mixed venous is responsible for normal tone of proximal pulmonary vascular segments; high alveolar is responsible for tone of distal segments. Bottom: hypoxia (breathing 10% O2 mixture). During hypoxia the mixed venous in proximal segment (A) undergoes little change, whereas alveolar decreases to a level that is not appreciably different from blood in distal segment (B); to the high tone of proximal segment is added the increase in tone of distal segment. Main component of pressor response to hypoxia is due to smooth muscle contraction in distal segment. FIo2, fraction of O2 in inspired gas.

From Fishman , by permission of the American Heart Association, Inc
Figure 25. Figure 25.

Calcium and smooth muscle contraction. A: block diagram of compartmentalization of Ca2+ in muscle fibers. Also shown are main pathways and transport systems for Na+ and Ca2+: 1) ATP‐dependent, ouabain‐sensitive Na+‐K+ exchange pump; 2) sarcolemmal Na+‐Ca2+ exchange mechanism (shown operating in forward or Ca2+ extrusion mode); 3) sarcoplasmic reticulum (SR) ATP‐dependent Ca2+ pump. Most of entering Na+ and Ca2+ is assumed to come through voltage‐sensitive conductance channels associated with action potential, k, Rate coefficient for fluxes of Na+ and Ca2+ across sarcolemma and sarcoplasmic reticulum membranes in directions indicated. B: contraction of vascular smooth muscle. When intracellular Ca2+ levels exceed a critical level (10−6 M), Ca2+ binds to calmodulin, a Ca2+‐binding protein; Ca2+‐calmodulin complex binds in turn to myosin kinase, thereby activating the enzyme. Active kinase then catalyzes phosphorylation of myosin, which can interact with actin to produce contraction. Cyclic AMP plays an important role in activating a cAMP‐dependent protein kinase that can transfer phosphate from ATP to proteins directly involved in regulation of intracellular Ca2+ levels and in interaction of actin with myosin.

A adapted from Blaustein
Figure 26. Figure 26.

Native resident of Lake Titicaca (Peruvian Andes, ∼4,500 m). Barrel chest is generally held to be one of several adaptations to life in rarified atmosphere.

Courtesy of R. B. Eckhardt
Figure 27. Figure 27.

Relation in Peruvian Andes between altitude, arterial O2 saturation , and mean pulmonary arterial pressure . Appreciable levels of arterial hypoxemia and of pulmonary hypertension occur at ∼3,000 m. During exercise (EX) arterial hypoxemia and pulmonary arterial pressure increase.

From Penaloza and Gamboa
Figure 28. Figure 28.

Effect of age on mean pulmonary arterial pressure at sea level and at altitude (Peruvian Andes).

From Penaloza and Gamboa
Figure 29. Figure 29.

Mean pulmonary arterial pressure and arterial O2 saturation (ART O2 SAT) in 3 groups of individuals. In healthy highlanders, arterial oxygenation is lower than in healthy sea‐level residents. This discrepancy is greatly widened in chronic alveolar hypoventilators (Monge's disease) at high altitude. Level of pulmonary arterial pressure is inversely related to degree of arterial hypoxemia.

Adapted from Heath and Williams
Figure 30. Figure 30.

A: schematic representations of bronchial circulation in different disorders. Top: bronchial arteries (BA). In chronic suppurative diseases of the lungs, bronchial arteries undergo considerable proliferation. Bottom: bronchial veins (BV). Proximal bronchial veins drain either into right atrium (RA) or left atrium (LA), depending on pressure levels in these 2 cardiac chambers. Normally most bronchial venous outflow from the lungs enters right atrium (thicker curved arrow). However, in right ventricular failure, bronchial venous drainage to left atrium increases. B, bronchus; C, expanded bronchial arterial circulation; PA, pulmonary artery. B: indicator‐dilution curves from pulmonary artery and brachial artery (BA) in a normal individual (left) and in a patient with bronchiectasis (right). Curves from the patient are identical in appearance, time, and height, indicating that catheter tip in pulmonary artery (in vicinity of bronchiectatic area) had sampled systemic arterial blood.a

A from Fishman , by permission of the American Heart Association, Inc. B from Cudkowicz
Figure 31. Figure 31.

Fetal circulation in the lamb. BCA, brachiocephalic artery; DA, ductus arteriosus; DV, ductus venosus; FO, foramen ovale; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RV, right ventricle; SVC, superior vena cava.a

From Dawes
Figure 32. Figure 32.

Schematic representation of changes in mean pulmonary arterial pressure, proportion of combined ventricular output (CVO) distributed to the lungs, actual pulmonary blood flow, and calculated pulmonary vascular resistance in fetal lambs during gestational development from 0.4 to 1.0 gestation. Progressive decrease in resistance is attributable to an increase in cross‐sectional area of pulmonary vascular bed, in large measure due to growth of new vessels.

From Rudolph . Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc
Figure 33. Figure 33.

Changes in patterns of pulmonary arterial (PA) pressure and flow after birth. Left: in the fetus. Right: after birth.

From Rudolph . Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc
Figure 34. Figure 34.

Schematic representation of effects of progressive restriction of pulmonary vascular bed by successive amputation of lobes of the lungs on mean pulmonary arterial (PA) pressure (assuming that pulmonary blood flow remains unchanged). Pneumonectomy (middle) evokes only a modest increase in pulmonary arterial pressure (to 22 mmHg). Subsequent removal of right lower and middle lobes leads to considerable pulmonary arterial hypertension (to 55 mmHg).

Data from Lategola
Figure 35. Figure 35.

Gut‐liver‐lung axis. Serotonin, brought to the liver via the portal vein, is partially removed by the liver. Removal is completed in the lungs.

Figure 36. Figure 36.

Influence of endothelium on responses of different vessels to acetylcholine (ACH). Increasing concentrations of acetylcholine were applied to rings of femoral, saphenous, splenic, and pulmonary arteries (circles) that had previously been contracted with norepinephrine. Those vessels in which endothelium was intact (solid curves) responded with increasing vasodilation. In vessels without endothelium (dashed curves), virtually no vasodilation occurred.

Adapted from De Mey and Vanhoutte


Figure 1.

gRenin‐angiotensin system. The lungs play a central role in control of systemic blood pressure because of the converting enzyme on the luminal aspect of pulmonary capillary endothelium. Strategic disposition of the enzyme and huge expanse of pulmonary capillary endothelium enable rapid and efficient conversion of angiotensin I to angiotensin II as blood courses through the lungs.



Figure 2.

Muscular pulmonary arteries (resistance vessels) in pulmonary circulation of various animal species. Elastic Van Gieson's stain. A: dog; × 500. B: cat; × 500. C: human; × 200. D: rat; × 800. A‐D: tunica media is relatively thin. E: guinea pig; × 200. Tunica media consists of crescentic masses of circular smooth muscle disposed in discontinuous segments resembling sphincters. In areas between sphincterlike masses of smooth muscle the wall consists only of an elastic lamina. F: cow; × 500. Tunica media is thick.

Micrographs courtesy of J. M. Kay


Figure 3.

Four‐quadrant diagram illustrating respiratory and circulatory adaptation by which O2 requirement is satisfied at rest (inner rectangle) and during exercise (outer rectangle). , concentration of O2 in arterial blood; Cvo2, concentration of O2 in venous blood; CAP area, capillary area; DL, diffusing capacity of the lungs; Hb, hemoglobin; , O2 capacity of hemoglobin; , mean alveolar O2 tension; , mean capillary O2 tension; , arterial O2 saturation; , venous O2 saturation.

Adapted from Barcroft


Figure 4.

Pulsatility in pulmonary circulation of the dog. A: transformation of pressure‐flow pulses along length of pulmonary circulation. Transmission time for pressure pulse from pulmonary artery to capillaries ∼0.09 s; from capillaries to veins, transmission time ∼0.03 s. B: top, changes in pulmonary blood volume of the dog at rest and exercise during a single cardiac cycle. Rate of change in pulmonary blood volume (striped area) equals difference between flows in main pulmonary artery and in pulmonary veins . Bottom, storage as calculated from discharge curves at consecutive sections of pulmonary vascular tree during a cardiac cycle. Spa, storage in pulmonary arteries; Spv, storage in pulmonary veins; ST, total storage. Most storage occurs within the pulmonary arterial tree. [A from Wiener, Fishman, et al. , by permission of the American Heart Association, Inc. B from Skalak, Fishman, et al. .]



Figure 5.

Propagation of pressure pulses (left) and flow pulses (right) through pulmonary circulation. Left: top and bottom curves, measured boundary pressures from which all other pressures and flows in the model were calculated. Dashed curves, sum of the mean pressure plus pressure oscillations propagated from right ventricle (arterial pulse). Solid curves include contribution of oscillatory part of left atrial pressure (venous pulse) and represent total (mean + arterial pulse + venous pulse) pressure at each location. Right: corresponding curves for flow. In contrast to left panel, for which top and bottom curves were determined experimentally, all curves in right panel were computed. Tracings, from top to bottom: main pulmonary artery, segmental pulmonary artery (generation 6), precapillaries, postcapillaries, segmental pulmonary vein (generation 38), and left atrium.

From Wiener, Fishman, et al. , by permission of the American Heart Association, Inc


Figure 6.

Principle of a Starling resistor. Thin‐walled collapsible tube traverses a closed chamber (A) in which pressure can be varied at will. Fluid flows from reservoir (R) into collecting vessel (striped area), traversing collapsible tube en route. When outflow pressure exceeds chamber pressure (left), flow is determined by difference between inflow and outflow pressure. However, when chamber pressure exceeds outflow pressure, so that collapsible tube closes (arrow), flow is determined by difference between inflow and chamber pressure.

Adapted from West et al.


Figure 7.

Zones of the lungs in different body positions as determined by interplay between pulmonary vascular (Ppv) and alveolar pressures (PA). For simplicity, only zones 1, 2, and 3 are shown. Ppa, pulmonary arterial pressure.a

Adapted from Hughes


Figure 8.

Blood flow in upright lung as function of vertical height.

Adapted from Glazier et al.


Figure 9.

Topographical distribution of pulmonary blood flow according to relationship among pulmonary arterial pressure (Ppa), pulmonary venous pressure (Ppv), and alveolar pressure (PA). Because of effect of surface tension, PA is more accurately pericapillary pressure. Zone 1 (apex): PA > Ppa > Ppv. No flow (except through corner vessels) because collapsible vessels close when pericapillary pressure exceeds the pressure inside the vessels. Vessels that close are capillaries and other alveolar vessels up to ∼30 μm diam. Zone 2: Ppa > PA > Ppv. Driving pressure is Ppa — PA. This difference increases down lung and so does flow. Zone 3: Ppa > Ppv > PA. Driving pressure is Ppa — Ppv. Although Ppa — Ppv does not change down lung, Ppa and Ppv continue to increase from top to bottom. Flow down zone 3 is less than zone 2. Zone 4 (appears at residual volume): this region of decreased flow appears during forced exhalation and has been attributed to either an increase in interstitial pressure at lung bases or to closure of small airways at low lung volumes as the increase in PA creates either zone 1 or zone 2 conditions.

Adapted from West et al. and Anthonisen and Milic‐Emili


Figure 10.

Alveolar, corner, and extra‐alveolar vessels. A: large extra‐alveolar artery (A) showing its muscle layer surrounded by a loose connective tissue sheath. Alveolar septa, inserted radially, presumably exert a radial outward pull that is responsible for dilation of these vessels as the lung is inflated. Lung parenchyma is characteristic of zone 2. a, Bundles of capillaries (corner vessels); b, flat septa containing open but smoothened, slitlike capillaries; c, septa containing completely closed (derecruited) capillaries. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. After 2 full inflations, peak arterial pressure = 11–12 mmHg, alveolar pressure = 10 mmHg. Thin epoxy section. B: bundle of wide‐open capillaries (a) within reversible folds of alveolar walls in a corner area. Bundles communicate with vessels (V) larger than capillaries, here probably a small nonmuscular artery that is part of the corner arrangement. Although this vessel cannot expand with inflation, it is also protected against collapse. In other locations, small veins are also visible in this arrangement. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. Thin epoxy section. C: capillaries inside a bundle of capillaries (a) in corner presumably connect small arteries with small veins (cf. B) and are protected against excess alveolar pressure. Arrangement is due to reversible pleating of alveolar walls. Some septal capillaries (b) are open but flattened, whereas others (c) are derecruited. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO4 into the pulmonary artery. Thin epoxy section. D: large extra‐alveolar vein (V) is surrounded by a loose connective tissue sheath. Bottom right, pleural surface. Normal rat lung fixed by instillation of fixatives into trachea after lung collapse. Relatively thick paraffin section, hematoxylin and eosin stain.

Micrographs courtesy of J. Gil


Figure 11.

Cross section of alveolar capillary from human lung lined by endothelium (EN). Endothelial nucleus is striking. Alveolar‐capillary barrier is organized into thick (right) and thin (left) portions. Thick side includes considerable interstitial space (IN), containing connective tissue elements, e.g., fibers (cf). In contrast, interstitial space on thin side is obliterated by fusion of basement membranes, which forms a minimal air‐blood barrier. C, capillary containing 3 red corpuscles in its lumen; EP, alveolar epithelium; F, fibroblast.

From Weibel


Figure 12.

Schematic representation of fascial sheath extending down wall of pulmonary arteriole.

Adapted from Hayek


Figure 13.

Pulmonary vascular pressures in consecutive segments of the pulmonary vascular tree and in comparable segments of a systemic artery. Measurements were made by direct puncture of arterial and venous segments of the subpleural microcirculation.

Adapted from Bhattacharya et al.


Figure 14.

Simultaneous tracings in the dog of pulmonary arterial and venous flow and pulmonary arterial and venous pressure. Variations in pulmonary arterial and venous flow are nearly simultaneous; maxima and minima in venous flow lag from corresponding points in arterial flow record only by the 0.09 s necessary for flow pulse to be propagated across pulmonary circulation.

From Morkin, Fishman, et al.


Figure 15.

Principle of determination of pulmonary wedge pressure. Pressure sensed by wedged catheter (left, balloon inflated) is same as that at conjunction of flowing (2 arrows) and static streams (distal to wedged catheter). Nonocclusive constriction distal to occlusive catheter does not affect determination of pulmonary wedge pressure. However, constriction distal to confluence, as in pulmonary venule (PV), may cause pulmonary wedge pressure to exceed left atrial (LA) pressure.

Adapted from Marini


Figure 16.

Effect of location of tip of wedged catheter on validity as measure of left atrial pressure (Pla); one catheter was wedged high (Pwh) and the other low (Pwl) in the lung. Initially the upper catheter was located in zone 2 of the lung and did not reflect left atrial pressure. Saline infusion increased left atrial pressure and converted lung containing upper wedged catheter to zone 3 conditions; both catheters then reflected left atrial pressures. Subsequent hemorrhage restored zone 2 conditions and original discrepancy between pulmonary wedge and left atrial pressures. Catheter that was wedged low operated throughout under zone 3 conditions.

From Todd et al.


Figure 17.

Effect of exercise on upright lung. Increase in mean pulmonary arterial pressure, coupled with increase in pulsatility, favors apical perfusion.

Adapted from West


Figure 18.

Pulmonary hemodynamics at rest and during steady‐state supine exercise in humans. A: normal males, avg age 23.6 ± 2.1 SD. B: normal females, avg age 23.8 ± 3.9 SD. BA, brachial arterial pressure; C.O., cardiac output; d, diastolic pressure; HR, heart rate; m, mean pressure; PAP, pulmonary arterial pressure; PCW, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; s, systolic pressure.

Adapted from Gurtner et al.


Figure 19.

Passive changes in pulmonary vascular resistance (R) at different levels of driving pressure and pulmonary blood flow (). Pulmonary venous pressure is assumed to remain constant. Pulmonary vascular resistance decreases as either blood flow or pressure drop increases.



Figure 20.

Pulmonary vascular pressure‐flow curves for detection of pulmonary vasomotor activity. A: theoretical basis for detecting pulmonary vasomotor activity with respect to passive pressure‐flow curves in the same individual. Solid line, passive pressure‐flow curve for the individual. Points A and B, linear incremental changes in pressure and flow along passive pressure‐flow curve. Point C, active change in pulmonary vascular resistance. B: practical application of passive pressure‐flow curves to detect vasomotor activity. Left: passive pressure‐flow curve has been established for the individual by measurements at 2 levels of blood flow, i.e., at rest and during exercise (EX). During a single trial of acute hypoxia, point falls above passive pressure‐flow curve, i.e., on a new curve that lies above the passive curve, suggesting that pulmonary vasoconstriction has occurred. Right: similar plot with calculated pulmonary vascular resistance instead of pressure drop as ordinate.

A courtesy of D. Silage


Figure 21.

Use of linear portions of a family of pulmonary vascular resistance curves as isopleths to display effect of test procedure on pulmonary vascular resistance. Right, resistance values (R units). At rest (•), pulmonary vascular resistance is higher at sea level than at altitude. During exercise (→), resistance values decrease in both instances, moving in each case to a lower resistance isopleth.



Figure 22.

Top: input impedance spectrum in main pulmonary artery of normal anesthetized dog. Pattern is similar to that of the ascending aorta but lower in amplitude. Minimal value of impedance modulus and crossover of impedance phase occurs at ∼6–8 Hz. Pulmonary hypertension secondary to valvular heart disease is associated with an increase in pulmonary arterial input impedance and a shift of minimal impedance modulus to right. Bottom: impedance phase. Flow in normal lung leads pressure at lower frequencies (negative phase); situation is reversed at higher frequencies.

Adapted from Milnor


Figure 23.

Arachidonic acid cascade, illustrating 2 pathways and some metabolic products able to change pulmonary vasomotor tone. Metabolic pathways of arachidonic acid initiated by cyclooxygenase and lipoxygenase catalyzed reactions. By stimulating a phospholipase the leukotrienes may in turn cause release of products of cyclooxygenase pathway.



Figure 24.

Putative sites of action of acute hypoxia. Pulmonary microvessel (artery, capillary, and vein) is shown traversing alveolar portion of the lung. Precapillary vessel is subdivided into proximal conducting segment (A), in which mixed venous blood (MVB ) affects some critical element of the vascular smooth muscle, and terminal segment (B), in which alveolar ordinarily is the major influence (striped area). Top: air breathing. Low mixed venous is responsible for normal tone of proximal pulmonary vascular segments; high alveolar is responsible for tone of distal segments. Bottom: hypoxia (breathing 10% O2 mixture). During hypoxia the mixed venous in proximal segment (A) undergoes little change, whereas alveolar decreases to a level that is not appreciably different from blood in distal segment (B); to the high tone of proximal segment is added the increase in tone of distal segment. Main component of pressor response to hypoxia is due to smooth muscle contraction in distal segment. FIo2, fraction of O2 in inspired gas.

From Fishman , by permission of the American Heart Association, Inc


Figure 25.

Calcium and smooth muscle contraction. A: block diagram of compartmentalization of Ca2+ in muscle fibers. Also shown are main pathways and transport systems for Na+ and Ca2+: 1) ATP‐dependent, ouabain‐sensitive Na+‐K+ exchange pump; 2) sarcolemmal Na+‐Ca2+ exchange mechanism (shown operating in forward or Ca2+ extrusion mode); 3) sarcoplasmic reticulum (SR) ATP‐dependent Ca2+ pump. Most of entering Na+ and Ca2+ is assumed to come through voltage‐sensitive conductance channels associated with action potential, k, Rate coefficient for fluxes of Na+ and Ca2+ across sarcolemma and sarcoplasmic reticulum membranes in directions indicated. B: contraction of vascular smooth muscle. When intracellular Ca2+ levels exceed a critical level (10−6 M), Ca2+ binds to calmodulin, a Ca2+‐binding protein; Ca2+‐calmodulin complex binds in turn to myosin kinase, thereby activating the enzyme. Active kinase then catalyzes phosphorylation of myosin, which can interact with actin to produce contraction. Cyclic AMP plays an important role in activating a cAMP‐dependent protein kinase that can transfer phosphate from ATP to proteins directly involved in regulation of intracellular Ca2+ levels and in interaction of actin with myosin.

A adapted from Blaustein


Figure 26.

Native resident of Lake Titicaca (Peruvian Andes, ∼4,500 m). Barrel chest is generally held to be one of several adaptations to life in rarified atmosphere.

Courtesy of R. B. Eckhardt


Figure 27.

Relation in Peruvian Andes between altitude, arterial O2 saturation , and mean pulmonary arterial pressure . Appreciable levels of arterial hypoxemia and of pulmonary hypertension occur at ∼3,000 m. During exercise (EX) arterial hypoxemia and pulmonary arterial pressure increase.

From Penaloza and Gamboa


Figure 28.

Effect of age on mean pulmonary arterial pressure at sea level and at altitude (Peruvian Andes).

From Penaloza and Gamboa


Figure 29.

Mean pulmonary arterial pressure and arterial O2 saturation (ART O2 SAT) in 3 groups of individuals. In healthy highlanders, arterial oxygenation is lower than in healthy sea‐level residents. This discrepancy is greatly widened in chronic alveolar hypoventilators (Monge's disease) at high altitude. Level of pulmonary arterial pressure is inversely related to degree of arterial hypoxemia.

Adapted from Heath and Williams


Figure 30.

A: schematic representations of bronchial circulation in different disorders. Top: bronchial arteries (BA). In chronic suppurative diseases of the lungs, bronchial arteries undergo considerable proliferation. Bottom: bronchial veins (BV). Proximal bronchial veins drain either into right atrium (RA) or left atrium (LA), depending on pressure levels in these 2 cardiac chambers. Normally most bronchial venous outflow from the lungs enters right atrium (thicker curved arrow). However, in right ventricular failure, bronchial venous drainage to left atrium increases. B, bronchus; C, expanded bronchial arterial circulation; PA, pulmonary artery. B: indicator‐dilution curves from pulmonary artery and brachial artery (BA) in a normal individual (left) and in a patient with bronchiectasis (right). Curves from the patient are identical in appearance, time, and height, indicating that catheter tip in pulmonary artery (in vicinity of bronchiectatic area) had sampled systemic arterial blood.a

A from Fishman , by permission of the American Heart Association, Inc. B from Cudkowicz


Figure 31.

Fetal circulation in the lamb. BCA, brachiocephalic artery; DA, ductus arteriosus; DV, ductus venosus; FO, foramen ovale; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RV, right ventricle; SVC, superior vena cava.a

From Dawes


Figure 32.

Schematic representation of changes in mean pulmonary arterial pressure, proportion of combined ventricular output (CVO) distributed to the lungs, actual pulmonary blood flow, and calculated pulmonary vascular resistance in fetal lambs during gestational development from 0.4 to 1.0 gestation. Progressive decrease in resistance is attributable to an increase in cross‐sectional area of pulmonary vascular bed, in large measure due to growth of new vessels.

From Rudolph . Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc


Figure 33.

Changes in patterns of pulmonary arterial (PA) pressure and flow after birth. Left: in the fetus. Right: after birth.

From Rudolph . Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc


Figure 34.

Schematic representation of effects of progressive restriction of pulmonary vascular bed by successive amputation of lobes of the lungs on mean pulmonary arterial (PA) pressure (assuming that pulmonary blood flow remains unchanged). Pneumonectomy (middle) evokes only a modest increase in pulmonary arterial pressure (to 22 mmHg). Subsequent removal of right lower and middle lobes leads to considerable pulmonary arterial hypertension (to 55 mmHg).

Data from Lategola


Figure 35.

Gut‐liver‐lung axis. Serotonin, brought to the liver via the portal vein, is partially removed by the liver. Removal is completed in the lungs.



Figure 36.

Influence of endothelium on responses of different vessels to acetylcholine (ACH). Increasing concentrations of acetylcholine were applied to rings of femoral, saphenous, splenic, and pulmonary arteries (circles) that had previously been contracted with norepinephrine. Those vessels in which endothelium was intact (solid curves) responded with increasing vasodilation. In vessels without endothelium (dashed curves), virtually no vasodilation occurred.

Adapted from De Mey and Vanhoutte
References
 1. Aarseth, P., L. Bjertnaes, And J. Karlsen. Changes in blood volume and extravascular water content in isolated perfused rat lungs during ventilation hypoxemia. Acta Physiol. Scand. 109: 61–67, 1980.
 2. Aarseth, P. and J. Karlsen. Blood volume and extravascular water content in the rat lung during acute alveolar hypoxia. Acta Physiol. Scand. 100: 236–245, 1977.
 3. Abdalla, M. A., and A. S. King. The functional anatomy of the bronchial circulation of the domestic fowl. J. Anat. 121: 537–550, 1976.
 4. Abraham, A. S., J. M. Kay, R. B. Cole, And A. C. Pincock. Hemodynamic and pathological study of the effect of chronic hypoxia and subsequent recovery of the heart and pulmonary vasculature of the rat. Cardiovasc. Res. 5: 95–102, 1971.
 5. Agostoni, E. and J. Piiper. Capillary pressure and distribution of vascular resistance in isolated lung. Am. J. Physiol. 202: 1033–1036, 1962.
 6. Agostoni, E., A. Taglietti, And I. Setnikar. Absorption force of the capillaries of the visceral pleura in determination of the intrapleural pressure. Am. J. Physiol. 191: 277–282, 1957.
 7. Ahmed, T., and W. Oliver, Jr. Does slow‐reacting substance of anaphylaxis mediate hypoxic pulmonary vasoconstriction? Am. Rev. Respir. Dis. 127: 566–571, 1983.
 8. Ahmed, T., W. Oliver, Jr., And A. Wanner. Variability of hypoxic pulmonary vasoconstriction in sheep. Role of prostaglandins. Am. Rev. Respir. Dis. 127: 59–62, 1983.
 9. Alexander, A. F. The bovine lung: normal vascular histology and vascular lesions in high mountain disease. Med. Thorac. 19: 528–542, 1962.
 10. Alexander, J. M., M. D. Nyby, And K. A. Jasberg. Prostaglandin synthesis inhibition restores hypoxic pulmonary vasoconstriction. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 903–908, 1977.
 11. Allison, D. J., and H. S. Stanbrook. A radiologic and physiologic investigation into hypoxic pulmonary vasoconstriction in the dog. Invest. Radiol. 15: 178–190, 1980.
 12. Anderson, F. L., and A. M. Brown. Pulmonary vasoconstriction elicited by stimulation of the hypothalamic integrative area for the defense reaction. Circ. Res. 21: 747–756, 1967.
 13. Anthonisen, N. R., and J. Milic‐Emili. Distribution of pulmonary perfusion in erect man. J. Appl. Physiol. 21: 760–766, 1966.
 14. Arborelius, M., Jr. Influence of moderate hypoxia in one lung on the distribution of the pulmonary circulation and ventilation. Scand. J. Clin. Lab. Invest. 17: 257–259, 1965.
 15. Arias‐Stella, J. and M. Saldana. The terminal portion of the pulmonary arterial tree in people native to high altitudes. Circulation 28: 915–925, 1963.
 16. Armstrong, D. J., and J. C. Luck. Accessibility of pulmonary stretch receptors from the pulmonary and bronchial circulations. J. Appl. Physiol. 36: 706–710, 1974.
 17. Assimacopoulos, A., R. Guggenheim, And Y. Kapanci. Changes in alveolar capillary configuration at different levels of lung inflation in the rat: an ultrastructural and morphometric study. Lab. Invest. 34: 10–22, 1976.
 18. Aviado, D. M. Anoxia and the pulmonary circulation: systemic mechanisms. In: The Lung Circulation. Oxford, UK: Pergamon, 1965, vol. 1, p. 3–83.
 19. Aviado, D. M., Jr., J. S. Ling, And C. F. Schmidt. Effects of anoxia on pulmonary circulation: reflex pulmonary vasoconstriction. Am. J. Physiol. 189: 253–262, 1957.
 20. Baile, E. M., J. M. B. Nelems, M. Schulzer, And P. D. Paré. Measurement of regional bronchial arterial blood flow and bronchovascular resistance in dogs. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 53: 1044–1049, 1982.
 21. Banister, J., and R. W. Torrance. The effects of tracheal pressure upon flow‐pressure relations in the vascular bed of isolated lungs. Q. J. Exp. Physiol. 45: 352–367, 1960.
 22. Barcroft, J. The Respiratory Function of the Lung. Lessons From High Altitudes. Cambridge, UK: Cambridge Univ. Press, pt. I, 1913.
 23. Barer, G. R. A comparison of the circulatory effects of angiotensin, vasopressin, and adrenaline in the anesthetized cat. J. Physiol. London 156: 49–66, 1961.
 24. Barer, G. R. Reactivity of the vessels of collapsed and ventilated lungs to drugs and hypoxia. Circ. Res. 18: 366–378, 1966.
 25. Barer, G. R., D. Bee, And R. A. Wach. Contribution of polycythaemia to pulmonary hypertension in simulated high altitude in rats. J. Physiol. London 336: 27–38, 1983.
 26. Barer, G. R., C. J. Emery, F. H. Mohammed, And I. P. Mungall. H1 and H2 histamine actions on lung vessels: their relevance to hypoxic vasoconstriction. Q. J. Exp. Physiol. 63: 157–169, 1978.
 27. Barer, G. R., P. Howard, J. R. McCurrie, And J. W. Shaw. Changes in the pulmonary circulation after bronchial occlusion in anesthetized dogs and cats. Circ. Res. 25: 747–764, 1969.
 28. Barer, G. R., P. Howard, And J. W. Shaw. Stimulus‐response curves for the pulmonary vascular bed to hypoxia and hypercapnia. J. Physiol. London 211: 139–155, 1970.
 29. Barer, G. R., and J. R. Mccurrie. Pulmonary vasomotor responses in the cat: the effects and interrelationships of drugs, hypoxia and hypercapnia. Q. J. Exp. Physiol. 54: 156–172, 1969.
 30. Barer, G. R., J. R. McCurrie, And J. W. Shaw. Effect of changes in blood pH on the vascular resistance in the normal and hypoxic cat lung. Cardiovasc. Res. 5: 490–497, 1971.
 31. Barer, G. R., and J. W. Shaw. Pulmonary vasodilator and vasoconstrictor actions of carbon dioxide. J. Physiol. London 213: 633–645, 1971.
 32. Barrett, C. T., M. A. Heymann, And A. M. Rudolph. Alpha and beta adrenergic receptor activity in fetal sheep. Am. J. Obstet. Gynecol. 112: 1114–1121, 1972.
 33. Bates, D. V., C. J. Varvis, R. E. Dowevan, And R. V. Christie. Variations in the pulmonary capillary blood volume and membrane diffusion component in health and disease. J. Clin. Invest. 39: 1401–1412, 1960.
 34. Beck, K. C. and J. Hildebrandt. Adaptation of vascular pressure‐flow‐volume hysteresis in isolated rabbit lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 671–679, 1983.
 35. Benjamin, J. J., P. S. Murtagh, D. F. Proctor, H. A. Menkes, And S. Permutt. Pulmonary vascular interdependence in excised dog lobes. J. Appl. Physiol. 37: 887–894, 1974.
 36. Benumof, J. L. Hypoxic pulmonary vasoconstriction and infusion of sodium nitroprusside. Anesthesiology 50: 481–483, 1979.
 37. Benumof, J. L. Mechanism of decreased blood flow to atelectatic lung. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 1047–1048, 1979.
 38. Benumof, J. L., J. M. Mathers, And E. A. Wahrenbrock. Cyclic hypoxic pulmonary vasoconstriction induced by concomitant carbon dioxide changes. J. Appl. Physiol. 41: 466–469, 1976.
 39. Bergel, D. H., and W. R. Milnor. Pulmonary vascular impedance in the dog. Circ. Res. 16: 401–415, 1965.
 40. Bergofsky, E. H. Mechanisms underlying vasomotor regulation or regional pulmonary blood flow in normal and disease states. Am. J. Med. 57: 378–397, 1974.
 41. Bergofsky, E. H. Active control of the normal pulmonary circulation. In: Lung Biology in Health and Disease. Pulmonary Vascular Diseases, edited by K. M. Moser, New York: Dekker, 1979, vol. 14, chapt. 3, p. 233–277.
 42. Bergofsky, E. H. Humoral control of the pulmonary circulation. Annu. Rev. Physiol. 42: 221–233, 1980.
 43. Bergofsky, E. H., B. G. Bass, R. Ferretti, And A. P. Fishman. Pulmonary vasoconstriction in response to precapillary hypoxemia. J. Clin. Invest. 42: 1201–1215, 1963.
 44. Bergofsky, E. H., F. Haas, And R. Porcelli. Determination of the sensitive vascular sites from which hypoxia and hypercapnia elicit rises in pulmonary arterial pressure. Federation Proc. 27: 1420–1425, 1968.
 45. Bergofsky, E. H. and S. Holtzman. A study of the mechanism involved in the pulmonary arterial pressor response to hypoxia. Circ. Res. 20: 506–519, 1967.
 46. Bergofsky, E. H., D. E. Lehr, And A. P. Fishman. The effect of changes in hydrogen ion concentration on the pulmonary circulation. J. Clin. Invest. 14: 1492–1502, 1962.
 47. Berkov, S. Hypoxic pulmonary vasoconstriction in the rat: the necessary role of angiotensin II. Circ. Res. 35: 257–261, 1974.
 48. Berryhill, R. E., and J. L. Benumof. PEEP‐induced discrepancy between pulmonary arterial wedge pressure and left atrial pressure: the effects of controlled vs. spontaneous ventilation and compliant vs. noncompliant lungs in the dog. Anesthesiology 31: 303–308, 1979.
 49. Beyne, J. Influence de l'anoxemie sur la grande circulation et sur la circulation pulmonaire. C. R. Soc. Biol. Paris 136: 399–400, 1942.
 50. Bhattacharya, J., S. Nanjo, And N. C. Staub. Factors affecting lung microvascular pressure. Ann. NY Acad. Sci. 384: 107–114, 1982.
 51. Bhattacharya, J., S. Nanjo, And N. C. Staub. Micropuncture measurement of lung microvascular pressure during 5–HT infusion. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 52: 634–637, 1982.
 52. Bjertnaes, L. J., A. Hauge, And T. Torgrimsen. The pulmonary vasoconstrictor response to hypoxia. The hypoxia‐sensitive site studied with a volatile inhibitor. Acta Physiol. Scand. 109: 447–462, 1980.
 53. Bland, R. D., R. Demling, S. Selinger, And N. C. Staub. Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep. Circ. Res. 40: 269–274, 1977.
 54. Blaustein, M. P. Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis. Am. J. Physiol. 232 (Cell Physiol.1): C165–C173, 1977.
 55. Boake, W. C., R. Daley, And I. K. R. McMillan. Observations on hypoxic pulmonary hypertension. Br. Heart J. 21: 31–39, 1959.
 56. Bohr, D. F. The pulmonary hypoxic response. State of the field. Chest 71, Suppl. 2: 244–246, 1977.
 57. Bohr, D. F. and B. Johansson. Contraction of vascular smooth muscle in response to plasma. Circ. Res. 19: 593–601, 1966.
 58. Bowers, R. E., K. Brigham, And P. J. Owen. Salicylate pulmonary edema. Mechanism in sheep and review of the clinical literature. Am. Rev. Respir. Dis. 115: 261–268, 1977.
 59. Bras, G., D. M. Berry, And P. Gyorgy. Plants as etiological factors in veno‐occlusive disease of the liver. Lancet 1: 960–962, 1957.
 60. Brashear, R. E., R. R. Martin, And J. C. Ross. In vivo histamine levels with hypoxia and compound 48/80. Am. J. Med. Sci. 260: 21–28, 1970.
 61. Braunwald, E., A. P. Fishman, And A. Cournand. Time relationship of dynamic events in the cardiac chambers, pulmonary artery and aorta in man. Ctrc. Res. 4: 100–107, 1956.
 62. Brigham, K. L., R. Bowers, And J. Haynes. Increased sheep lung vascular permeability caused by Escherichia coli endotoxin. Circ. Res. 45: 292–297, 1979.
 63. Brigham, K. L., R. E. Bowers, And P. J. Owen. Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability. J. Clin. Invest. 58: 391–398, 1976.
 64. Brigham, K. L., T. R. Harris, And P. J. Owen. [14C]urea and [14C]sucrose as permeability indicators in histamine pulmonary edema. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 99–101, 1977.
 65. Brigham, K. L., and P. J. Owen. Increased sheep lung vascular permeability caused by histamine. Circ. Res. 37: 647–657, 1975.
 66. Brigham, K. L., and P. J. Owen. Mechanism of the serotonin effect on lung transvascular fluid and protein movement in awake sheep. Circ. Res. 36: 761–770, 1975.
 67. Brody, J. S., E. J. Stemmler, And A. B. Dubois. Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins. J. Clin. Invest. 47: 783–799, 1968.
 68. Brutsaert, D. Influence of reserpine and of adrenolytic agents on the pulmonary arterial pressor response to hypoxia and catecholamines. Arch. Int. Physiol. Biochim. 72: 395–412, 1964.
 69. Brutsaert, D. The effects of reserpine and adrenolytic agents on the pulmonary arterial pressor response to serotonin. Exp. Med. Surg. 23: 13–27, 1965.
 70. Bryan, A. C., L. G. Bentivoglio, F. Beerel, H. Macleish, A. Zidulka, And D. V. Bates. Factors affecting regional distribution of ventilation and perfusion in the lung. J. Appl. Physiol. 19: 395–402, 1964.
 71. Burns, J. Heart and pulmonary arteries in rats fed on Senecio jacobaea. J. Pathol. 106: 187–194, 1972.
 72. Butler, J., and H. W. Paley. Lung volume and pulmonary circulation. Med. Thorac. 19: 261–267, 1962.
 73. Butler, W. H., A. R. Mattocks, And J. M. Barnes. Lesions in the liver and lungs in rats given pyrrole derivatives of pyrrolizidine alkaloids. J. Pathol. 100: 169–175, 1970.
 74. Byrne‐Quinn, E., and R. F. Grover. Aminorex (Menocil) and amphetamine: acute and chronic effects on pulmonary and systemic haemodynamics in the calf. Thorax 27: 127–131, 1972.
 75. Calka, W. Vascular supply of the lungs through direct branches of the aorta in domestic pig. Folia Morphol. Warsaw Engl. Transl. 34: 135–142, 1975.
 76. Campbell, A. G. M., F. Cockburn, G. S. Dawes, And J. E. Milligan. Pulmonary vasoconstriction in asphyxia during cross‐circulation between twin foetal lambs. J. Physiol. London 192: 111–121, 1967.
 77. Campbell, A. G. M., G. S. Dawes, A. P. Fishman, And A. I. Hyman. Pulmonary vasoconstriction and changes in heart rate during asphyxia in immature foetal lambs. J. Physiol. London 192: 93–110, 1967.
 78. Campbell, A. G. M., G. S. Dawes, A. P. Fishman, A. I. Hyman, And A. M. Perks. The release of a bradykinin‐like pulmonary vasodilator substance in foetal and new‐born lambs. J. Physiol. London 195: 83–96, 1968.
 79. Cassidy, S. S., F. A. Gaffney, And R. L. Johnson, Jr. A perspective on PEEP. N. Engl. J. Med. 304: 421–422, 1981.
 80. Cassin, S., G. S. Dawes, J. C. Mott, B. B. Ross, And L. B. Strang. The vascular resistance of the foetal and newly ventilated lung of the lamb. J. Physiol. London 171: 61–79, 1964.
 81. Cassin, S., G. S. Dawes, And B. B. Ross. Pulmonary blood flow and vascular resistance in immature foetal lambs. J. Physiol. London 171: 80–89, 1964.
 82. Casteels, R., K. Kitamura, H. Kuriyama, And H. Suzuki. The membrane properties of the smooth muscle cells of the rabbit main pulmonary artery. J. Physiol. London 271: 41–61, 1977.
 83. Casteels, R., K. Kitamura, H. Kuriyama, And H. Suzuki. Excitation‐contraction coupling in the smooth muscle cells of the rabbit main pulmonary artery. J. Physiol. London 271: 63–79, 1977.
 84. Chesney, C. F., and J. R. Allen. Endocardial fibrosis associated with monocrotaline‐induced pulmonary hypertension in nonhuman primates (Macaca arctoides). Am. J. Vet. Res. 34: 1577–1581, 1973.
 85. Chiesa, A., G. Ciappi, L. Balbi, And L. Chiandussi. Role of various causes of arterial desaturation in liver cirrhosis. Clin. Sci. 37: 803–814, 1969.
 86. Coceani, F., I. Bishai, E. White, E. Bodach, And P. M. Olley. Action of prostaglandins, endoperoxides, and thromboxanes on the lamb ductus arteriosus. Am. J. Physiol. 234 (Heart Circ. Physiol. 3): H117–H122, 1978.
 87. Colebatch, H. J. H. Adrenergic mechanisms in the effects of histamine in the pulmonary circulation of the cat. Circ. Res. 26: 379–396, 1970.
 88. Colebatch, H. J. H., G. S. Dawes, J. W. Goodwin, And R. A. Nadeau. The nervous control of the circulation in the foetal and newly expanded lungs of the lamb. J. Physiol. London 178: 544–562, 1965.
 89. Coleridge, J. C. G. and C. Kidd. Relationship between pulmonary arterial pressure and impulse activity in pulmonary arterial baroreceptor fibres. J. Physiol. London 158: 197–205, 1961.
 90. Collins, R., and J. A. Maccario. Blood flow in the lung. J. Biomech. 12: 373–395, 1979.
 91. Cournand, A. Air and blood. In: Circulation of the Blood. Men and Ideas, edited by A. P. Fishman and D. W. Richards. New York: Oxford Univ. Press, 1964, p. 3–70.
 92. Cournand, A., H. L. Motley, L. Werko, And D. W. Richards, Jr. Physiological studies of the effects of intermittent positive pressure breathing on cardiac output in man. Am. J. Physiol. 152: 162–174, 1948.
 93. Crandall, E. D., And R. W. Flumerfelt. Effects of time‐varying blood flow on oxygen uptake in the pulmonary capillaries. J. Appl. Physiol. 23: 944–953, 1967.
 94. Cudkowicz, L. Bronchial arterial circulation in man: normal anatomy and responses to disease. In: Lung Biology in Health and Disease. Pulmonary Vascular Diseases, edited by K. M. Moser. New York: Dekker, 1979, vol. 14, chapt. 2, p. 111–232.
 95. Cudkowicz, L., and D. G. Wraith. A method of study of the pulmonary circulation in finger clubbing. Thorax 12: 313–321, 1957.
 96. Culver, B. H. and J. Butler. Mechanical influences on the pulmonary microcirculation. Annu. Rev. Physiol. 42: 187–198, 1980.
 97. Cumming, G., R. Henderson, K. Horsfield, And S. S. Singhal. The functional morphology of the pulmonary circulation. In: Pulmonary Circulation and Interstitial Space, edited by A. P. Fishman and H. H. Hecht. Chicago, IL: Univ. of Chicago Press, 1969, p. 327–340.
 98. Daly, I. de B., and M. de B. Daly. The effects of stimulation of the carotid body chemoreceptors on the pulmonary vascular bed in the dog: the vasosensory controlled perfused living animal preparation. J. Physiol. London 148: 201–219, 1959.
 99. Daly, I. de B., and M. de B. Daly. The nervous control of the pulmonary circulation. In: Problems of Pulmonary Circulation, edited by A. V. S. de Reuck and M. O'Connor. Boston, MA: Little, Brown, 1961, p. 44–60. (Ciba Found. Study Group 8.)
 100. Daly, I. de B., and C. O. Hebb. Pulmonary and Bronchial Vascular Systems. London: Arnold, 1966.
 101. Daly, I. de B., C. C. Michel, D. J. Ramsay, And B. A. Waaler. Conditions governing the pulmonary vascular response to ventilation hypoxia and hypoxaemia in the dog. J. Physiol. London 196: 351–379, 1968.
 102. Daoud, F. S., J. T. Reeves, And J. W. Schaffer. Failure of hypoxic pulmonary vasoconstriction in patients with liver cirrhosis. J. Clin. Invest. 51: 1076–1080, 1972.
 103. Davies, G. and L. Reid. Growth of the alveoli and pulmonary arteries in childhood. Thorax 25: 669–681, 1970.
 104. Dawes, G. S. Physiological changes in the circulation after birth. In: Circulation of the Blood. Men and Ideas, edited by A. P. Fishman and D. W. Richards. New York: Oxford Univ. Press, 1964, p. 743–816.
 105. Dawes, G. S. Fetal and Neonatal Physiology. Chicago, IL: Year Book, 1968, p. 98.
 106. Dawes, G. S., and J. C. Mott. The vascular tone of the foetal lung. J. Physiol. London 164: 465–477, 1962.
 107. Dawson, C. A., D. J. Grimm, And J. H. Lineham. Effects of lung inflation on longitudinal distribution of pulmonary vascular resistance. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 1089–1092, 1977.
 108. Dawson, C. A., D. J. Grimm, And J. H. Linehan. Influence of hypoxia on the longitudinal distribution of pulmonary vascular resistance. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 493–498, 1978.
 109. Dawson, C. A., D. J. Grimm, And J. H. Linehan. Lung inflation and longitudinal distribution of pulmonary vascular resistance during hypoxia. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47: 532–536, 1979.
 110. Dawson, C. A., R. L. Jones, And L. H. Hamilton. Hemodynamic responses of isolated cat lungs during forward and retrograde perfusion. J. Appl. Physiol. 35: 95–102, 1973.
 111. Dawson, C. A., J. H. Linehan, And D. A. Rickaby. Pulmonary microcirculatory hemodynamics. Ann. NY Acad. Sci. 384: 90–105, 1982.
 112. Deal, E. C., Jr., E. R. McFadden, Jr., R. H. Ingram, Jr., And J. J. Jaeger. Esophageal temperature during exercise in asthmatic and nonasthmatic subjects. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 484–490, 1979.
 113. De Mey, J. G., and P. M. Vanhoutte. Role of the intima in cholinergic and purinergic relaxation of isolated canine femoral arteries. J. Physiol. London 316: 347–355, 1981.
 114. De Mey, J. G., and P. M. Vanhoutte. Heterogeneous behavior of the canine arterial and venous wall. Importance of the endothelium. Circ. Res. 51: 439–447, 1982.
 115. Denison, D., J. Ernsting, And D. I. Fryer. The effect of the inverted posture upon the distribution of blood flow in man. J. Physiol. London 172: 49–50, 1964.
 116. Detar, R. Mechanism of physiological hypoxia‐induced depression of vascular smooth muscle contraction. Am. J. Physiol. 238 (Heart Circ. Physiol. 7): H761–H769, 1980.
 117. Detar, R., and D. F. Bohr. Oxygen and vascular smooth muscle contraction. Am. J. Physiol. 214: 241–244, 1968.
 118. Detar, R., and D. F. Bohr. Contractile responses of isolated vascular smooth muscle during prolonged exposure to anoxia. Am. J. Physiol. 222: 1269–1277, 1972.
 119. Detar, R. and M. Gellai. Oxygen and isolated vascular smooth muscle from the main pulmonary artery of the rabbit. Am. J. Physiol. 221: 1791–1794, 1971.
 120. DeWitt, D. L., J. S. Day, W. K. Sonnenburg, And W. L. Smith. Concentrations of prostaglandin endoperoxide synthase and prostaglandin I2 synthase in the endothelium and smooth muscle of bovine aorta. J. Clin. Invest. 72: 1882–1888, 1983.
 121. Dexter, L., J. L. Whittenberger, F. W. Haynes, W. T. Goodale, R. Gorlin, And C. G. Sawyer. Effect of exercise on circulatory dynamics of normal individuals. J. Appl. Physiol. 3: 439–453, 1951.
 122. Doekel, R. C., E. K. Weir, R. Looga, R. F. Grover, And J. T. Reeves. Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 76–80, 1978.
 123. Downing, S. E., and T. H. Gardner. Cephalic and carotid reflex influences on cardiac function. Am. J. Physiol. 215: 1192–1199, 1968.
 124. Downing, S. E., and J. C. Lee. Nervous control of the pulmonary circulation. Annu. Rev. Physiol. 42: 199–210, 1980.
 125. Dugard, A. and A. Naimark. Effect of hypoxia on distribution of pulmonary blood flow. J. Appl. Physiol. 23: 663–671, 1967.
 126. Duke, H. N. The site of action of anoxia on the pulmonary blood vessels of the cat. J. Physiol. London 125: 373–382, 1954.
 127. Duke, H. N., and E. M. Killick. Pulmonary vasomotor responses of isolated perfused cat lungs to anoxia. J. Physiol. London 117: 303–316, 1952.
 128. Dunham, B. M., G. A. Grindlinger, T. Utsunomiya, M. M. Krausz, H. B. Hechtman, And D. Shepro. Role of prostaglandins in positive end‐expiratory pressure‐induced negative inotropism. Am. J. Physiol. 241 (Heart Circ. Physiol. 10): H783–H788, 1981.
 129. Ellsworth, M. L., T. J. Gregory, And J. C. Newell. Pulmonary prostacyclin production with increased flow and sympathetic stimulation. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 1225–1231, 1983.
 130. Emery, C. J., D. Bee, And G. R. Barer. Mechanical properties and reactivity of vessels in isolated perfused lungs of chronically hypoxic rats. Clin. Sci. 61: 569–580, 1981.
 131. Emery, C. J., P. J. M. Sloan, F. H. Mohammed, And G. R. Barer. The action of hypercapnia during hypoxia on pulmonary vessels. Bull. Eur. Physiopathol. Respir. 13: 763–776, 1977.
 132. Enson, Y., C. Giuntini, M. L. Lewis, T. Q. Morris, M. I. Ferrer, And R. M. Harvey. The influence of hydrogen ion concentration and hypoxia on the pulmonary circulation. J. Clin. Invest. 43: 1146–1162, 1964.
 133. Euler, U. S. von, And G. Liljestrand. Observations on the pulmonary arterial blood pressure in the cat. Acta Physiol. Scand. 12: 301–320, 1946.
 134. Falch, D. K., and S. B. Stromme. Pulmonary blood volume and interventricular circulation time in physically trained and untrained subjects. Eur. J. Appl. Physiol. Occup. Physiol. 40: 211–218, 1979.
 135. Fay, F. S. Guinea pig ductus arteriosus. I. Cellular and metabolic basis for oxygen sensitivity. Am. J. Physiol. 221: 470–479, 1971.
 136. Feisal, K., J. Soni, And A. Dubois. Pulmonary circulation time, pulmonary arterial blood volume, and the ratio of gas to tissue volume in the lungs of dogs. J. Clin. Invest. 41: 390–400, 1962.
 137. Fishman, A. P. The clinical significance of the pulmonary collateral circulation. Circulation 24: 677–690, 1961.
 138. Fishman, A. P. Respiratory gases in the regulation of the pulmonary circulation. Physiol. Rev. 41: 214–280, 1961.
 139. Fishman, A. P. Dynamics of the pulmonary circulation. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Bethesda, MD: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 48, p. 1667–1743.
 140. Fishman, A. P. Pulmonary edema. The water‐exchanging function of the lung. Circulation 46: 390–408, 1972.
 141. Fishman, A. P. Dietary pulmonary hypertension. Circ. Res. 35: 657–660, 1974.
 142. Fishman, A. P. Hypoxia on the pulmonary circulation: how and where it acts. Circ. Res. 38: 221–231, 1976.
 143. Fishman, A. P. (editor). Pulmonary Diseases and Disorders. New York: McGraw‐Hill, 1980.
 144. Fishman, A. P., H. W. Fritts, Jr, and A. Cournand. Effects of acute hypoxia and exercise on the pulmonary circulation. Circulation 22: 204–215, 1960.
 145. Fishman, A. P., J. Mcclement, A. Himmelstein, And A. Cournand. Effects of acute anoxia on the circulation and respiration in patients with chronic pulmonary disease studied during the steady state. J. Clin. Invest. 31: 770–781, 1952.
 146. Fishman, A. P., and G. G. Pietra. Handling of bioactive materials by the lung. Pt. 1. N. Engl. J. Med. 291: 884–889, 1974.
 147. Fishman, A. P., and G. G. Pietra. Handling of bioactive materials by the lung. Pt. 2. N. Engl. J. Med. 291: 953–959, 1974.
 148. Fishman, A. P., and G. G. Pietra. Vasodilator treatment of primary pulmonary hypertension. In: Update: Pulmonary Diseases and Disorders, edited by A. P. Fishman. New York: McGraw‐Hill, 1982, p. 396–408.
 149. Forrest, J. B., and A. Fargas‐Babjak. Variability of the pulmonary vascular response to hypoxia and relation to gas exchange in dogs. Can. Anaesth. Soc. J. 25: 479–487, 1978.
 150. Fournier, P., J. Mensch‐Dechène, B. Ranson‐Bitker, W. Valladares, And A. Lockhart. Effects of sitting up on pulmonary blood pressure, flow, and volume in man. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 36–40, 1979.
 151. Fowler, K. T., J. B. West, And M. C. F. Pain. Pressure flow characteristics of horizontal lung preparations of minimal height. Respir. Physiol. 1: 88–98, 1966.
 152. Frank, G. W., and J. A. Bevan. Electrical stimulation causes endothelium‐dependent relaxation in lung vessels. Am. J. Physiol. 244 (Heart Circ. Physiol. 13): H793–H798, 1983.
 153. Freedman, M. E., G. L. Snider, P. Brostoff, S. Kimelblot, And L. N. Katz. Effects of training on response of cardiac output to muscular exercise in athletes. J. Appl. Physiol. 8: 37–47, 1955.
 154. Fried, R., B. Meyrick, M. Rabinovitch, And L. Reid. Polycythemia and the acute hypoxic response in awake rats following chronic hypoxia. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 1167–1172, 1983.
 155. Fritts, H. W., Jr., P. Harris, R. H. Clauss, J. E. Odell, And A. Cournand. The effect of acetylcholine on the human pulmonary circulation under normal and hypoxic conditions. J. Clin. Invest. 37: 99–108, 1958.
 156. Fuchs, K. I., L. G. Moore, And S. Rounds. Pulmonary vascular reactivity is blunted in pregnant rats. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 703–707, 1982.
 157. Fung, Y. C., and S. S. Sobin. Elasticity of the pulmonary alveolar sheet. Circ. Res. 30: 451–469, 1972.
 158. Fung, Y. C., and S. S. Sobin. Pulmonary alveolar blood flow. Circ. Res. 30: 470–490, 1972.
 159. Fung, Y.‐C. B., and S. S. Sobin. Pulmonary alveolar blood flow. In: Lung Biology in Health and Disease. Bioengineering Aspects of the Lung, edited by J. B. West. New York: Dekker, 1977, vol. 3, chapt. 4, p. 267–359.
 160. Furchgott, R. F. Role of endothelium in responses of vascular smooth muscle. Circ. Res. 53: 557–573, 1983.
 161. Gaar, K. A., Jr., A. E. Taylor, L. J. Owens, And A. C. Guyton. Effect of capillary pressure and plasma protein on development of pulmonary edema. Am. J. Physiol. 213: 79–82, 1967.
 162. Gabel, J. C., and R. E. Drake. Pulmonary capillary pressure in intact dog lungs. Am. J. Physiol. 235 (Heart Circ. Physiol. 4): H569–H573, 1978.
 163. Gehr, P., M. Bachofen, And E. R. Weibel. The normal human lung: ultrastructure and morphometric estimation of diffusion capacity. Respir. Physiol. 32: 121–140, 1978.
 164. Gerber, J. G., N. Voelkel, A. S. Nies, I. F. McMurtry, And J. T. Reeves. Moderation of hypoxic vasoconstriction by infused arachidonic acid: role of PGI2. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 49: 107–112, 1980.
 165. Gil, J. Influence of surface forces on pulmonary circulation. In: Pulmonary Edema, edited by A. P. Fishman and E. M. Renkin. Bethesda, MD: Am. Physiol. Soc., 1979, p. 53–64.
 166. Gil, J. Organization of microcirculation in the lung. Annu. Rev. Physiol. 42: 177–186, 1980.
 167. Gil, J. Alveolar and extraalveolar connective tissue compartments and origin of pulmonary lymph. Microcirculation 1: 407–420, 1981.
 168. Gil, J. Alveolar wall relations. Ann. NY Acad. Sci. 384: 31–43, 1982.
 169. Gil, J., and E. R. Weibel. Morphological study of pressure‐volume hysteresis in rat lungs fixed by vascular perfusion. Respir. Physiol. 15: 190–213, 1972.
 170. Gilbert, R. D., J. R. Hessler, D. V. Eitzman, And S. Cassin. Site of pulmonary vascular resistance in fetal goats. J. Appl. Physiol. 32: 47–53, 1972.
 171. Gillis, C. N. Metabolism of vasoactive hormones by lung. Anesthesiology 39: 626–632, 1973.
 172. Glaister, D. H. Effect of acceleration. In: Regional Differences in the Lung, edited by J. B. West. New York: Academic, 1977, p. 331–346.
 173. Glauser, F. L., R. P. Fairman, J. E. Millen, And R. K. Falls. Indomethacin blunts ethchlorvynol‐induced pulmonary hypertension but not pulmonary edema. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 563–566, 1982.
 174. Glazier, J. B., J. M. B. Hughes, J. E. Maloney, And J. B. West. Measurements of capillary dimensions and blood volume in rapidly frozen lungs. J. Appl. Physiol. 26: 65–76, 1969.
 175. Glazier, J. B., and J. F. Murray. Site of pulmonary vasomotor reactivity in the dog during alveolar hypoxia and serotonin and histamine infusion. J. Clin. Invest. 50: 2550–2558, 1971.
 176. Goldberg, S. J., R. A. Levy, B. Siassi, And J. Betten. Effects of maternal hypoxia and hyperoxia upon the neonatal pulmonary vasculature. Pediatrics 48: 528–533, 1971.
 177. Goldring, R. M., G. M. Turino, D. H. Andersen, And A. P. Fishman. Cor pulmonale in cystic fibrosis of the pancreas (Abstract). Circulation 24: 942, 1961.
 178. Goldring, R. M., G. M. Turino, G. Cohen, A. G. Jameson, B. G. Bass, And A. P. Fishman. The catecholamines in the pulmonary arterial pressor response to acute hypoxia. J. Clin. Invest. 41: 1211–1221, 1962.
 179. Gorsky, B. H., and T. C. Lloyd Jr.. Effects of perfusate composition on hypoxic vasoconstriction in isolated lung lobes. J. Appl. Physiol. 23: 683–686, 1967.
 180. Graham, R., C. Skoog, L. Oppenheimer, J. Rabson, And H. S. Goldberg. Critical closure in the canine pulmonary vasculature. Circ. Res. 50: 566–572, 1982.
 181. Gray, B. A., D. R. Mccaffree, E. D. Sivak, And H. T. Mccurdy. Effect of pulmonary vascular engorgement on respiratory mechanics in the dog. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 45: 119–127, 1978.
 182. Green, J. F., and N. D. Schmidt. Mechanism of hyperpnea induced by changes in pulmonary blood flow. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 56: 1418–1422, 1984.
 183. Grimm, D. J., C. A. Dawson, T. S. Hakim, And J. H. Linehan. Pulmonary vasomotion and the distribution of vascular resistance in a dog lung lobe. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 545–550, 1978.
 184. Grover, R. F., J. H. K. Vogel, K. H. Averill, And S. G. Blount Jr.. Pulmonary hypertension: individual and species variability relative to vascular reactivity (Editorial). Am. Heart J. 66: 1–3, 1963.
 185. Gruetter, C. A., D. B. Mcnamara, A. L. Hyman, And P. J. Kadowitz. Contractile responses of intrapulmonary vessels from three species to arachidonic acid and an epoxymethano analog of PGH2. Can. J. Physiol. Pharmacol. 56: 206–215, 1978.
 186. Guintini, C., A. Maseri, And R. Bianchi. Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects. J. Clin. Invest. 45: 1770–1789, 1966.
 187. Gurtner, H. P. Hypertensive pulmonary vascular disease: some remarks on its incidence and aetiology. In: Proc. Meet. Eur. Soc. Study Drug Toxic, 12th, Uppsala, 1970, edited by S. B. Baker. Amsterdam: Excerpta Med., 1971, p. 81–88.
 188. Gurtner, H. P. L'hypertension pulmonaire apres absorption d'un anorexigene, le fumarate d'aminorex. Rev. Med. Paris 14: 911–920, 1974.
 189. Gurtner, H. P., P. Walser, And E. Fassler. Normal values for pulmonary hemodynamics at rest and during exercise in man. Prog. Respir. Res. 9: 295–315, 1975.
 190. Haas, F., and E. H. Bergofsky. Role of the mast cell in the pulmonary pressor response to hypoxia. J. Clin. Invest. 51: 3154–3162, 1972.
 191. Hakim, T. S., C. A. Dawson, And J. H. Linehan. Hemodynamic responses of dog lung lobe to lobar venous occlusion. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47: 145–152, 1979.
 192. Hakim, T. S., R. P. Michel, And H. K. Chang. Partitioning of pulmonary vascular resistance in dogs by arterial and venous occlusion. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 710–715, 1982.
 193. Hales, C. A. and H. Kazemi. Role of histamine in the hypoxic vascular response of the lung. Respir. Physiol. 24: 81–88, 1975.
 194. Hales, C. A., E. T. Rouse, And H. Kazemi. Failure of saralasin acetate, a competitive inhibitor of angiotensin II, to diminish alveolar hypoxic vasoconstriction in the dog. Cardiovasc. Res. 11: 541–546, 1977.
 195. Hales, C. A., E. T. Rouse, And J. L. Slate. Influence of aspirin and indomethacin on variability of alveolar hypoxic vasoconstriction. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 33–39, 1978.
 196. Hales, C. A., L. Sonne, M. Peterson, D. Kong, M. Miller, And W. D. Watkins. Role of thromboxane and prostacyclin in pulmonary vasomotor changes after endotoxin in dogs. J. Clin. Invest. 68: 497–505, 1981.
 197. Hales, C. A., and D. M. Westphal. Pulmonary hypoxic vasoconstriction: not affected by chemical sympathectomy. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 529–533, 1979.
 198. Hamasaki, Y., M. Mojarad, And S. I. Said. Relaxant action of VIP on cat pulmonary artery: comparison with acetylcholine, isoproterenol, and PGE1. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 1607–1611, 1983.
 199. Hamasaki, Y., H.‐H. Tai, And S. I. Said. Hypoxia stimulates prostacyclin generation by dog lung in vitro. Prostaglandins Leukotrienes Med. 8: 311–316, 1982.
 200. Hamilton, W. F., and E. A. Lombard. Intrathoracic volume changes in relation to the cardiopneumogram. Circ. Res. 1: 76–82, 1953.
 201. Hanna, C. J., M. K. Bach, P. D. Pare, And R. R. Schellenberg. Slow‐reacting substances (leukotrienes) contract human airway and pulmonary vascular smooth muscle in vitro. Nature London 290: 343–344, 1981.
 202. Harris, P. and D. Heath. The effect of drugs. In: The Human Pulmonary Circulation. Baltimore, MD: Williams & Wilkins, 1977, p. 113–126.
 203. Harris, R. H., M. Zmudka, Y. Maddox, P. W. Ramwell, And J. R. Fletcher. Relationships of TXB2 and 6‐keto‐PGF1α to the hemodynamic changes during baboon endotoxic shock. Adv. Prostaglandin Thromboxane Res. 7: 843–849, 1980.
 204. Harvey, R. M., Y. Enson, R. Betti, M. L. Lewis, D. F. Rochester, And M. I. Ferrer. Further observations on the effect of hydrogen ion on the pulmonary circulation. Circulation 35: 1019–1027, 1967.
 205. Hauge, A. Conditions governing the pressor response to ventilation hypoxia in isolated perfused rat lungs. Acta Physiol. Scand. 72: 33–44, 1968.
 206. Hauge, A. Hypoxia and pulmonary vascular resistance: the relative effects of pulmonary arterial and alveolar PO2. Acta Physiol. Scand. 76: 121–130, 1969.
 207. Hauge, A., and K. L. Melmon. Role of histamine in hypoxic pulmonary hypertension in the rat. II. Depletion of histamine, serotonin, and catecholamines. Circ. Res. 22: 385–392, 1968.
 208. Hauge, A., and N. C. Staub. Prevention of hypoxic vasoconstriction in cat lung by histamine‐releasing agent 48/80. J. Appl. Physiol. 26: 693–699, 1969.
 209. Hayek, H. von. The Human Lung. New York: Hafner, 1960.
 210. Heath, D., C. Edwards, M. Winson, And P. Smith. Effects on the right ventricle, pulmonary vasculature, and carotid bodies of the rat of exposure to, and recovery from, simulated high altitude. Thorax 28: 24–28, 1973.
 211. Heath, D., P. Smith, D. Williams, P. Harris, J. Arias‐Stella, And H. Kruger. The heart and pulmonary vasculature of the llama (Lama glama). Thorax 29: 463–471, 1974.
 212. Heath, D., and D. R. Williams. Man at High Altitude. The Pathophysiology of Acclimatization and Adaptation (2nd ed.). New York: Churchill Livingstone, 1981.
 213. Heath, D., D. Williams, P. Harris, P. Smith, H. Krüger, And A. Ramirez. The pulmonary vasculature of the mountain‐viscacha (Lagidium peruanum). The concept of adapted and acclimatized vascular smooth muscle. J. Comp. Pathol. 91: 293–301, 1981.
 214. Hebb, C. Motor innervation of the pulmonary blood vessels of mammals. In: Pulmonary Circulation and Interstitial Space, edited by A. P. Fishman and H. H. Hecht. Chicago, IL: Univ. of Chicago Press, 1969, p. 195–222.
 215. Hedenstierna, G., F. C. White, R. Mazzone, And P. D. Wagner. Redistribution of pulmonary blood flow in the dog with PEEP ventilation. J. Appl Physiol.: Respirat. Environ. Exercise Physiol. 46: 278–287, 1979.
 216. Heffner, J. E., S. A. Shoemaker, E. M. Canham, M. Patel, I. F. McMurtry, H.G. Morris, And J. E. Repine. Acetyl glyceryl ether phosphorylcholine‐stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2. J. Clin. Invest. 71: 351–357, 1983.
 217. Heinemann, H. O., and A. P. Fishman. Nonrespiratory functions of mammalian lung. Physiol. Rev. 49: 1–47, 1969.
 218. Herget, J., and F. PaleôEK. Experimental chronic pulmonary hyertension. In: International Review of Experimental Pathology, edited by G. W. Richter and M. A. Epstein. New York: Academic, 1978, vol. 18, p. 347–406.
 219. Herget, J., A. J. Suggett, E. Leach, And G. R. Barer. Resolution of pulmonary hypertension and other features induced by chronic hypoxia in rats during complete and intermittent normoxia. Thorax 33: 468–473, 1978.
 220. Heusner, A. A. Body size, energy metabolism, and the lungs. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 54: 867–873, 1983.
 221. Heymann, M. A., and A. M. Rudolph. Control of the ductus arteriosus. Physiol. Rev. 55: 62–78, 1975.
 222. Heymann, M. A., and A. M. Rudolph. Effects of acetylsalicylic acid on the ductus arteriosus and circulation in fetal lambs in utero. Cire. Res. 38: 418–422, 1976.
 223. Heymann, M. A., A. M. Rudolph, A. S. Nies, And K. L. Melmon. Bradykinin production associated with oxygenation of the fetal lamb. Circ. Res. 25: 521–534, 1969.
 224. Hislop, A. and L. Reid. New findings in pulmonary arteries of rats with hypoxia‐induced pulmonary hypertension. Br. J. Exp. Pathol. 57: 542–554, 1976.
 225. Hoffman, E. A., S. J. Lai‐Fook, J. Wei, And E. H. Wood. Regional pleural surface expansile forces in intact dogs by wick catheters. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 55: 1523–1529, 1983.
 226. Hoffman, E. A., M. L. Munroe, A. Tucker, And J. T. Reeves. Histamine H1‐ and H2‐receptors in the cat and their roles during alveolar hypoxia. Respir. Physiol. 29: 255–264, 1977.
 227. Holcroft, J. W., D. D. Trunkey, And M. A. Carpenter. Sepsis in the baboon: factors affecting resuscitation and pulmonary edema in animals resuscitated with Ringer's lactate versus Plasmanate. J. Trauma 17: 600–610, 1977.
 228. Holloway, H., M. Perry, J. Downey, J. Parker, And A. Taylor. Estimation of effective pulmonary capillary pressure in intact lungs. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 54: 846–851, 1983.
 229. Hopkins, R. A., J. W. Hammon, Jr., P. A. Mchale, P. K. Smith, And R. W. Anderson. Pulmonary vascular impedance analysis of adaptation to chronically elevated blood flow in the awake dog. Circ. Res. 45: 267–274, 1979.
 230. Horsfield, K. Morphometry of the small pulmonary arteries in man. Circ. Res. 42: 593–597, 1978.
 231. Howard, P., G. R. Barer, B. Thompson, P. M. Warren, C. J. Abbott, And I. P. F. Mungall. Factors causing and reversing vasoconstriction in unventilated lung. Respir. Physiol 24: 325–345, 1975.
 232. Howell, J. B. L., S. Permutt, D. F. Proctor, And R. L. Riley. Effect of inflation of the lung on different parts of pulmonary vascular bed. J. Appl. Physiol. 16: 71–76, 1961.
 233. Hughes, J. M. B. Pulmonary circulation and fluid balance. In: Respiratory Physiology II, edited by J. G. Widdicombe. Baltimore, MD: University Park, 1977, vol. 14, p. 135–183. (Int. Rev. Physiol. Ser.)
 234. Hunter, C., G. R. Barer, J. W. Shaw, And E. J. Clegg. Growth of the heart and lungs in hypoxic rodents. A model of human hypoxic diseases. Clin. Sci. Mol. Med. 46: 375–391, 1974.
 235. Hüttemeier, P. C., W. D. Watkins, M. B. Peterson, And W. M. Zapol. Acute pulmonary hypertension and lung thromboxane release after endotoxin infusion in normal and leukopenic sheep. Circ. Res. 50: 688–694, 1982.
 236. Huval, W. V., M. A. Mathieson, L. I. Stemp, B. M. Dunpam, A. G. Jones, D. Shepro, And H. D. Hechtman. Therapeutic benefits of 5‐hydroxytryptamine inhibition following pulmonary embolism. Ann. Surg. 197: 220–225, 1983.
 237. Hyman, A. L., and P. S. Kadowitz. Effects of alveolar and perfusion hypoxia and hypercapnia on pulmonary vascular resistance in the lamb. Am. J. Physiol. 228: 397–403, 1975.
 238. Hyman, A. L., E. W. Spannhake, And P. J. Kadowitz. Divergent responses to arachidonic acid in the feline pulmonary vascular bed. Am. J. Physiol 239 (Heart Circ. Physiol. 8): H40–H46, 1980.
 239. Ingram, R. H., J. P. Szidon, And A. P. Fishman. Response of the main pulmonary artery of dogs to neuronally released versus blood‐borne norepinephrine. Circ. Res. 26: 249–269, 1970.
 240. Ingram, R. H., J. P. Szidon, R. Skalak, And A. P. Fishman. Effects of sympathetic nerve stimulation on the pulmonary arterial tree of the isolated lobe perfused in situ. Circ. Res. 22: 801–815, 1968.
 241. Jameson, A. G. Gaseous diffusion from alveoli into pulmonary arteries. J. Appl. Physiol. 19: 448–456, 1964.
 242. Jardin, F., J. Farcot, L. Boisante, N. Curien, A. Margairaz, And J. Bourdarias. Influence of positive end‐expiratory pressure on left ventricular performance. N. Engl J. Med. 304: 387–392, 1981.
 243. Jobsis, F. F. What is a molecular oxygen sensor? What is a transduction process? Adv. Exp. Med. Biol. 78: 3–18, 1977.
 244. Johansson, B. Determinants of vascular reactivity. Federation Proc. 33: 121–126, 1974.
 245. Kabins, S. A., J. Fridman, J. Neustadt, G. Espinosa, And L. N. Katz. Mechanisms leading to lung edema in pulmonary embolization. Am. J. Physiol. 198: 543–546, 1960.
 246. Kadowitz, P. J., C. A. Gruetter, F. W. Spannhake, And A. C. Hyman. Pulmonary vascular responses to prostaglandins. Federation Proc. 40: 1991–1996, 1981.
 247. Kadowitz, P. J., P. D. Joiner, And A. L. Hyman. Effect of prostaglandin E2 on pulmonary vascular resistance in intact dog, swine and lamb. Eur. J. Pharmacol. 31: 72–80, 1975.
 248. Kaneko, K., J. Milic‐Emili, M. B. Dolovich, A. Dawson, And D. V. Bates. Regional distribution of ventilation and perfusion as a function of body position. J. Appl. Physiol 21: 767–777, 1966.
 249. Kapanci, Y., A. Assimacopoulos, C. Irle, A. Zwahlen, And G. Gabbiani. “Contractile interstitial cells” in pulmonary alveolar septa: a possible regulator of ventilation/perfusion ratio? J. Cell Biol. 60: 375–392, 1974.
 250. Kapanci, Y., and P. M. Costabella. Studies on structure and function of contractile interstitial cells (CIC) in pulmonary alveolar septa (Abstract). Federation Proc. 38: 964, 1979.
 251. Kapanci, Y., P. M. Costabella, P. Cerutti, And A. Assimacopoulos. Distribution and function of cytoskeletal proteins in lung cells with particular reference to “contractile interstitial cells”. Methods Achiev. Exp. Pathol. 9: 147–168, 1979.
 252. Kay, J. M., and R. F. Grover. Lung mast cells and hypoxic pulmonary hypertension. Prog. Respir. Res. 9: 157–164, 1975.
 253. Kay, J. M. and D. Heath. Crotalaria Spectabilis. The Pulmonary Hypertension Plant. Springfield, IL: Thomas, 1969, 136 p.
 254. Kay, J. M., P. M. Keane, K. L. Suyama, And D. Gauthier. Angiotensin converting enzyme activity and evolution of pulmonary vascular disease in rats with monocrotaline pulmonary hypertension. Thorax 37: 88–96, 1982.
 255. Kay, J. M., P. Smith, And D. Heath. Aminorex and the pulmonary circulation. Thorax 26: 262–270, 1971.
 256. Kay, J. M., J. C. Waymire, And R. F. Grover. Lung mast cell hyperplasia and pulmonary histamine‐forming capacity in hypoxic rats. Am. J. Physiol. 226: 178–184, 1974.
 257. Kazemi, H., P. E. Bruecke, And E. F. Parsons. Role of autonomic nervous system in the hypoxic response of the pulmonary vascular bed. Respir. Physiol. 15: 245–254, 1972.
 258. King, R. J. Pulmonary surfactant. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 1–8, 1982.
 259. Knoblauch, A., A. Sybert, N. J. Brennan, J. T. Sylvester, And G. H. Gurtner. Effect of hypoxia and CO on a cytochrome P‐450‐mediated reaction in rabbit lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 1635–1642, 1981.
 260. Korner, P. I., and S. W. White. Circulatory control in hypoxia by sympathetic nerves and adrenal medulla. J. Physiol. London 184: 272–290, 1966.
 261. Koyama, T. and M. Horimoto. Pulmonary microcirculatory response to localized hypercapnia. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 53: 1556–1564, 1982.
 262. Koyama, T., S. Nakajima, And Y. Kakiuchi. Quick increase of pulmonary blood flow in response to an acute alveolar hypoxia in human subjects. Jpn. J. Physiol. 27: 1–11, 1977.
 263. Kuida, H., H. H. Hecht, R. L. Lange, A. M. Brown, T. J. Tsagaris, And J. L. Thorne. Brisket disease. III. Spontaneous remission of pulmonary hypertension and recovery from heart failure. J. Clin. Invest. 42: 589–596, 1964.
 264. Kuramoto, K. and S. Rodbard. Effects of blood flow and left atrial pressure on pulmonary venous resistance. Circ. Res. 11: 240–246, 1962.
 265. Lai‐Fook, S. J. A continuum mechanics analysis of pulmonary vascular interdependence in isolated dog lobes. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 419–429, 1979.
 266. Lai‐Fook, S. J., and R. E. Hyatt. Effect of parenchyma and length changes on vessel pressure‐diameter behavior in pig lungs. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 47: 666–669, 1979.
 267. Lammerant, J. Le volume sanguin des poumons. Brussels: Arscia, 1957.
 268. Landis, E. M., and J. R. Pappenheimer. Exchange of substances through the capillary walls. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Bethesda, MD: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 29, p. 961–1034.
 269. Lategola, M. T. Pressure‐flow relationships in the dog lung during acute, subtotal pulmonary vascular occlusion. Am. J. Physiol. 192: 613–619, 1958.
 270. Lauweryns, J. M., and A. Van Lommel. Morphometric analysis of hypoxia‐induced synaptic activity in intrapulmonary neuroepithelial bodies. Cell Tissue Res. 226: 201–214, 1982.
 271. Leach, E., P. Howard, And G. R. Barer. Resolution of hypoxic changes in the heart and pulmonary arterioles during intermittent correction of hypoxia. Clin. Sci. Mol Med. 52: 153–162, 1977.
 272. Leffler, C. W., and J. R. Hessler. Pulmonary and systemic effects of exogenous prostaglandin I2 in fetal lambs. Eur. J. Pharmacol. 54: 37–42, 1979.
 273. Leffler, C. W., T. L. Tyler, And S. Cassin. Effect of indomethacin on pulmonary vascular response to ventilation of fetal goats. Am. J. Physiol. 234 (Heart Circ. Physiol. 3): H346–H351, 1978.
 274. Leier, C. V., D. Bambach, S. Nelson, J. B. Hermiller, P. Huss, R. Magorien, And D. V. Unverferth. Captopril in primary pulmonary hypertension. Circulation 67: 155–161, 1983.
 275. Levin, D. L., L. J. Mills, M. Parkey, J. Garriott, And W. Campbell. Constriction of the fetal ductus arteriosus after administration of indomethacin to the pregnant ewe. J. Pediatr. 94: 647–650, 1979.
 276. Levin, D. L., A. M. Rudolph, M. A. Heymann, And R. H. Phibbs. Morphological development of the pulmonary vascular bed in fetal lambs. Circulation 53: 144–151, 1976.
 277. Levitzky, M. G. Chemoreceptor stimulation and hypoxic pulmonary vasoconstriction in conscious dogs. Respir. Physiol. 37: 151–160, 1979.
 278. Lewin, R. J., C. E. Cross, P. Rieben, And P. F. Salisbury. Stretch reflexes from the main pulmonary artery to the systemic circulation. Circ. Res. 9: 585–588, 1961.
 279. Lewis, A. B., M. A. Heymann, And A. M. Rudolph. Gestational changes in pulmonary vascular responses in fetal lambs in utero. Circ. Res. 39: 536–541, 1976.
 280. Lewis, M. L., and L. C. Christianson. Behavior of the human pulmonary circulation during head‐up tilt. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 45: 249–254, 1978.
 281. Leysen, J. E. Serotonergic receptors in brain tissue: properties and identification of various 3H‐ligand binding sites in vitro. J. Physiol. Paris 77: 351–362, 1981.
 282. Liebow, A. A. Recent observations on pulmonary collateral circulation. Med. Thorac. 19: 609–622, 1962.
 283. Liljestrand, G. Chemical control of distribution of pulmonary blood flow. Acta Physiol. Scand. 44: 216–240, 1958.
 284. Lilker, E. S., and E. J. Nagy. Gas exchange in the pulmonary collateral circulation of dogs. Am. Rev. Respir. Dis. 112: 615–620, 1975.
 285. Linehan, J. H., and C. A. Dawson. A three‐compartment model of the pulmonary vasculature: effects of vasoconstriction. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 55: 923–928, 1983.
 286. Lloyd, T. C. Jr.. Effect of alveolar hypoxia on pulmonary vascular resistance. J. Appl. Physiol. 19: 1086–1094, 1964.
 287. Lloyd, T. C. Jr.. Role of nerve pathways in the hypoxic vasoconstriction of the lung. J. Appl. Physiol. 21: 1351–1355, 1966.
 288. Lloyd, T. C. Jr.. Influences of Po2 and pH on resting and active tensions of pulmonary arterial strips. J. Appl. Physiol. 22: 1101–1109, 1967.
 289. Lloyd, T. C. Jr.. Hypoxic pulmonary vasoconstriction: role of perivascular tissue. J. Appl. Physiol. 25: 560–565, 1968.
 290. Lloyd, T. C. Jr.. Effect of increased intracranial pressure on pulmonary vascular resistance. J. Appl. Physiol. 35: 332–335, 1973.
 291. Lock, J. E., P. M. Olley, And F. Coceani. Direct pulmonary vascular responses to prostaglandins in the conscious newborn lamb. Am. J. Physiol. 238 (Heart Circ. Physiol. 7): H631–H638, 1980.
 292. Lock, J. E., P. M. Olley, And F. Coceani. Enhanced ã‐adrenergic‐receptor responsiveness in hypoxic neonatal pulmonary circulation. Am. J. Physiol. 240 (Heart Circ. Physiol. 9): H697–H703, 1981.
 293. Lockhart, A. Functional aspects of the pulmonary collateral circulation. In: Pulmonary Circulation in Health and Disease, edited by G. Cumming and G. Bonsignore. New York: Plenum, 1980, p. 43–65.
 294. Lockhart, A. Pressure‐flow‐volume relationships in the normal human pulmonary circulation at sea‐level and at altitude. In: Pulmonary Circulation in Health and Disease, edited by G. Cumming and G. Bonsignore. New York: Plenum, 1980, p. 337–355.
 295. Lockhart, A., M. Zelter, J. Mensch‐Dechene, G. Antezana, M. Paz‐Zamora, E. Vargas, And J. Coudert. Pressure‐flow‐volume relationships in pulmonary circulation of normal highlanders. J. Appl. Physiol. 41: 449–456, 1976.
 296. Lopez‐Muniz, R., N. L. Stephens, B. Bromberger‐Barnea, S. Permutt, And R. Riley. Critical closure of pulmonary vessels analyzed in terms of Starling resistor model. J. Appl. Physiol. 24: 625–635, 1968.
 297. Macklin, C. C. Evidence of increase in the capacity of the pulmonary arteries and veins of dogs, cats and rabbits during inflation of the freshly excised lung. Rev. Can. Biol. 5: 199–232, 1946.
 298. Magno, M. G., and A. P. Fishman. Origin, distribution, and blood flow of bronchial circulation in anesthetized sheep. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 272–279, 1982.
 299. Malik, A. B. Pulmonary vascular response to increase in intracranial pressure: role of sympathetic mechanisms. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335–343, 1977.
 300. Malik, A. B. The role of metabolic acidosis in the pulmonary vascular response to hemorrhage and shock. J. Trauma 18: 108–114, 1978.
 301. Malik, A. B. Pulmonary microembolism. Physiol. Rev. 63: 1114–1207, 1983.
 302. Malik, A. B., and B. S. L. Kidd. Adrenergic blockade on the pulmonary vascular response to hypoxia. Respir. Physiol. 19: 96–106, 1973.
 303. Malik, A. B., and B. S. L. Kidd. Independent effects of changes in H+ and CO2 concentrations on hypoxic pulmonary vasoconstriction. J. Appl. Physiol. 34: 318–323, 1973.
 304. Malik, A. B., and B. S. L. Kidd. Time course of pulmonary vascular response to hypoxia in dogs. Am. J. Physiol. 224: 1–6, 1973.
 305. Malik, A. B., and S. E. Tracy. Bronchovascular adjustments after pulmonary embolism. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 49: 476–481, 1980.
 306. Marini, J. J. Respiratory Medicine and Intensive Care. Baltimore, MD: Williams & Wilkins, 1981.
 307. Marshall, B. E. and C. Marshall. Continuity of response to hypoxic pulmonary vasoconstriction. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 49: 189–196, 1980.
 308. Martin, L. F., A. Tucker, M. L. Munroe, And J. T. Reeves. Lung mast cells and hypoxic pulmonary vasoconstriction in cats. Respiration 35: 73–77, 1978.
 309. Mattocks, A. R. Toxicity of pyrrolizidine alkaloids. Nature London 217: 723–728, 1968.
 310. May, N. D. S. Anatomy of the Sheep (3rd ed.). St. Lucia, Australia: Univ. of Queensland Press, 1970.
 311. Mazzone, R. W. Influence of vascular and transpulmonary pressures on the functional morphology of the pulmonary microcirculation. Microvasc. Res. 20: 295–306, 1980.
 312. Mazzone, R. W., C. M. Durand, And J. B. West. Electron microscopy of lung rapidly frozen under controlled physiological conditions. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 325–333, 1978.
 313. McDonald, D. A. Blood Flow in Arteries. London: Arnold, 1974.
 314. McDonald, I. G. and J. Butler. Distribution of vascular resistance in the isolated perfused dog lung. J. Appl. Physiol. 23: 463–474, 1967.
 315. McDonald, J. W. D., M. Ali, E. Morgan, E. R. Townsend, And J. D. Cooper. Thomboxane synthesis by sources other than platelets in association with complement‐induced pulmonary leukostasis and pulmonary hypertension in sheep (Abstract). Circ. Res. 52: 1–6, 1983.
 316. McFadden, E. R. Jr.. Respiratory heat and water exchange: physiological and clinical implications. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 331–336, 1983.
 317. McMahon, S. M., D. F. Proctor, And S. Permutt. Pleural surface pressure in dogs. J. Appl. Physiol. 27: 881–885, 1969.
 318. McMurtry, I. F., A. B. Davidson, J. T. Reeves, And R. F. Grover. Inhibition of hypoxic pulmonary vasoconstriction by calcium antagonists in isolated rat lungs. Circ. Res. 38: 99–104, 1976.
 319. McMurtry, I. F., K. G. Morris, And M. D. Petrun. Blunted hypoxic vasoconstriction in lungs from short‐term high‐altitude rats. Am. J. Physiol. 238 (Heart Circ. Physiol. 7): H849–H857, 1980.
 320. McMurtry, I. F., M. D. Petrun, And J. T. Reeves. Lungs from chronically hypoxic rats have decreased pressor response to acute hypoxia. Am. J. Physiol. 235 (Heart Circ. Physiol. 4): H104–H109, 1978.
 321. McMurtry, I. F., M. D. Petrun, A. Tucker, And J. T. Reeves. Pulmonary vascular reactivity in the spontaneously hypertensive rat. Blood Vessels 16: 61–70, 1979.
 322. McMurtry, I. F., J. T. Reeves, D. H. Will, And R. F. Grover. Reduction of bovine pulmonary hypertension by normoxia, verapamil and hexaprenaline. Experientia 33: 1192–1194, 1977.
 323. McMurtry, I. F., S. Rounds, And H. S. Stanbrook. Studies of the mechanism of hypoxic pulmonary vasoconstriction. Adv. Shock. Res. 8: 21–33, 1982.
 324. Mead, J. Mechanical properties of lungs. Physiol. Rev. 41: 281–330, 1961.
 325. Mead, J., T. Takishima, And D. Leith. Stress distribution in lungs: a model of pulmonary elasticity. J. Appl. Physiol. 28: 596–608, 1970.
 326. Mellemgaard, K., K. Winkler, N. Tygstrup, And J. Georg. Sources of venoarterial admixture in portal hypertension. J. Clin. Invest. 42: 1399–1405, 1963.
 327. Meyrick, B., K. Fujiwara, And L. Reid. Smooth muscle myosin in precursor and mature smooth muscle cells in normal pulmonary arteries and the effect of hypoxia. Exp. Lung Res. 2: 303–313, 1981.
 328. Meyrick, B., W. Gamble, And L. Reid. Development of Crotalaria pulmonary hypertension: hemodynamic and structural study. Am. J. Physiol. 239 (Heart Circ. Physiol.8): H692–H702, 1980.
 329. Meyrick, B. and L. Reid. The effect of continued hypoxia on rat pulmonary arterial circulation. An ultrastructural study. Lab. Invest. 38: 188–200, 1978.
 330. Meyrick, B. and L. Reid. Hypoxia and incorporation of 3H‐thymidine by cells of the rat pulmonary arteries and alveolar wall. Am. J. Pathol. 96: 51–70, 1979.
 331. Meyrick, B. and L. Reid. Ultrastructural features of the distended pulmonary arteries of the normal rat. Anat. Rec. 193: 71–98, 1979.
 332. Milic‐Emili, J., and N. M. Siafakas. The nature of zone 4 in regional distribution of pulmonary blood flow. In: Pulmonary Circulation in Health and Disease, edited by G. Cumming and G. Bonsignore. New York: Plenum, 1980, p. 211–224.
 333. Miller, M. A., and C. A. Hales. Role of cytochrome P‐450 in alveolar hypoxic pulmonary vasoconstriction in dogs. J. Clin. Invest. 64: 666–673, 1979.
 334. Milnor, W. R. Hemodynamics. Baltimore, MD: Williams & Wilkins, 1982.
 335. Milnor, W. R., D. H. Bergel, And J. D. Bargainer. Hydraulic power associated with pulmonary blood flow and its relation to heart rate. Circ. Res. 19: 467–480, 1966.
 336. Milsom, W. K., B. L. Langille, And D. R. Jones. Vagal control of pulmonary vascular resistance in the turtle Chrysemys scripta. Can. J. Zool. 55: 359–367, 1977.
 337. Mitzner, W., and J. T. Sylvester. Hypoxic vasoconstriction and fluid filtration in pig lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 1065–1071, 1981.
 338. Mitzner, W., J. T. Sylvester, And Y. K. Ngeow. Evidence for hypoxic constriction of alveolar vessels (Abstract). Physiologist 23: 154, 1980.
 339. Modell, H. I., K. Beck, And J. Butler. Functional aspects of canine bronchial‐pulmonary vascular communications. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 50: 1045–1051, 1981.
 340. Moore, L. G., I. F. McMurtry, And J. T. Reeves. Effects of sex hormones on cardiovascular and hematologic responses to chronic hypoxia in rats. Proc. Soc. Exp. Biol. Med. 158: 658–662, 1978.
 341. Moore, L. G., and J. T. Reeves. Pregnancy blunts pulmonary vascular reactivity in dogs. Am. J. Physiol. 239 (Heart Circ. Physiol. 8): H297–H301, 1980.
 342. Moret, P. R. Coronary blood flow and myocardial metabolism in man at high altitude. In: High Altitude Physiology. Cardiac and Respiratory Aspects, edited by R. Porter and J. Knight. London: Churchill Livingstone, 1971, p. 131–148. (Ciba Found. Symp.)
 343. Moret, P., E. Covarrubias, J. Coudert, And F. Duchosal. Cardiocirculatory adaptation to chronic hypoxia: comparative study of coronary flow, myocardial oxygen consumption and efficiency between sea level and high altitude residents. Acta Cardiol. 27: 283–305, 1972.
 344. Morkin, E., J. A. Collins, H. S. Goldman, And A. P. Fishman. Pattern of blood flow in the pulmonary veins of the dog. J. Appl. Physiol. 20: 1118–1128, 1965.
 345. Morkin, E., O. R. Levine, And A. P. Fishman. Pulmonary capillary flow pulse and the site of pulmonary vasoconstriction in the dog. Circ. Res. 15: 146–160, 1964.
 346. Morris, H. R., P. J. Piper, G. W. Taylor, Amd J. R. Tippins. The role of arachidonate lipoxygenase in the release of SRS‐A from guinea‐pig chopped lung. Prostaglandins 19: 371–383, 1980.
 347. Motulsky, J. H., M. D. Snavely, R. J. Hughes, And P. A. Insel. Interaction of verapamil and other calcium channel blockers with α1‐ and α2‐adrenergic receptors. Circ. Res. 52: 226–231, 1983.
 348. Nakamura, T., S. Nakamura, T. Tazawa, S. Abe, T. Aikawa, And K. Tokita. Measurement of blood flow through portopulmonary anastomosis in portal hypertension. J. Lab. Clin. Med. 65: 114–121, 1965.
 349. Nandiwada, P. A., A. L. Hyman, And P. J. Kadowitz. Pulmonary vasodilator responses to vagal stimulation and acetylcholine in the cat. Circ. Res. 53: 86–95, 1983.
 350. Nayar, H. S., R. M. Mathur, And V. V. Ranade. The role of serotonin (5‐hydroxytryptamine) in the pulmonary arterial pressor response during acute hypoxia. Indian J. Med. Res. 60: 1665–1673, 1972.
 351. Newell, J. C., M. G. Levitzky, J. A. Krasney, And R. E. Dutton. Phasic reflux of pulmonary blood flow in atelectasis: influence of systemic Po2. J. Appl. Physiol. 40: 883–888, 1976.
 352. Newman, J. H., N. F. Voelkel, C. M. Arroyave, And J. T. Reeves. Distribution of mast cells and histamine in canine pulmonary arteries. Respir. Physiol. 40: 191–198, 1980.
 353. Nihill, M. R., D. G. Mcnamara, And R. L. Vick. The effects of increased blood viscosity on pulmonary vascular resistance. Am. Heart J. 92: 65–72, 1976.
 354. Okada, R. D., G. M. Pohost, H. D. Kirshenbaum, F. G. Kushner, C. A. Boucher, P. C. Block, And H. W. Strauss. Radionuclide‐determined change in pulmonary blood volume with exercise. Improved sensitivity of multigated blood‐pool scanning in detecting coronary‐artery disease. N. Engl. J. Med. 301: 569–576, 1979.
 355. Olley, P. M. and F. Coceani. Prostaglandins and the ductus arteriosus. Annu. Rev. Med. 32: 375–385, 1981.
 356. Orchard, C. H., R. S. De leon, And M. K. Sykes. The relationship between hypoxic pulmonary vasoconstriction and arterial oxygen tension in the intact dog. J. Physiol. London 338: 64–74, 1983.
 357. O'Rourke, M. F. Vascular impedance in studies of arterial and cardiac function. Physiol. Rev. 62: 570–623, 1982.
 358. Osswald, W. and S. Guimaraes. Adrenergic mechanisms in blood vessels: morphological and pharmacological aspects. Rev. Physiol. Biochem. Pharmacol. 96: 54–122, 1983.
 359. Overholser, K. A., J. Bhattacharya, And N. C. Staub. Microvascular pressures in the isolated, perfused dog lung: comparison between theory and measurement. Microvasc. Res. 23: 67–76, 1982.
 360. Overland, E. S., R. N. Gupta, G. J. Huchon, And J. F. Murray. Measurement of pulmonary tissue volume and blood flow in persons with normal and edematous lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 1375–1383, 1981.
 361. Owen, D. A. A. Histamine receptors in the cardiovascular system. Gen. Pharmacol. 8: 141–156, 1977.
 362. Pace, J. B., R. H. Cox, F. Alvarez‐Vara, And G. Karreman. Influence of sympathetic nerve stimulation on pulmonary hydraulic input power. Am. J. Physiol. 222: 196–201, 1972.
 363. Parker, J. C., A. C. Guyton, And A. E. Taylor. Pulmonary interstitial and capillary pressures estimated from intra‐alveolar fluid pressures. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267–276, 1978.
 364. Parker, J. C., P. R. Kvietys, K. P. Ryan, And A. E. Taylor. Comparison of isogravimetric and venous occlusion capillary pressures in isolated dog lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 964–968, 1983.
 365. Parker, J. C., R. E. Parker, D. N. Granger, And A. E. Taylor. Vertical gradient in regional vascular resistance and pre to postcapillary resistance ratios in the dog lung. Lymphology 12: 191–200, 1979.
 366. Parker, R. E., D. N. Granger, B. H. Cook, H. J. Granger, And A. E. Taylor. A histochemical analysis of vascular and nonvascular smooth muscles in the canine lung. Microvasc. Res. 18: 167–174, 1979.
 367. Parker, R. E., D. N. Granger, And A. E. Taylor. Estimates of isogravimetric capillary pressures during alveolar hypoxia. Am. J. Physiol. 241 (Heart Circ. Physiol. 10): H732–H739, 1981.
 368. Parratt, J. R., and R. M. Sturgess. Evidence that prostaglandin release mediates pulmonary vasoconstriction induced by E. coli endotoxin (Abstract). J. Physiol. London 246: 79P–80P, 1975.
 369. Patel, D. J., D. P. Schilder, And A. J. Mallos. Mechanical properties and dimensions of the major pulmonary arteries. J. Appl. Physiol. 15: 92–96, 1960.
 370. Peake, M. D., A. L. Harabin, N. J. Brennan, And J. T. Sylvester. Steady‐state vascular responses to graded hypoxia in isolated lungs of five species. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 1214–1219, 1981.
 371. Pease, R. D., J. L. Benumof, And F. R. Trousdale. PAO2 and Pvo2 interaction on hypoxic pulmonary vasoconstriction. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 134–139, 1982.
 372. Peñaloza, D. and R. Gamboa. Hipertension pulmonar. In: Cardiologia Pediátrica. Madrid: Salvat, in press.
 373. Peñaloza, D., I. Sime, N. Banchero, And R. Gamboa. Pulmonary hypertension in healthy men born and living at high altitude. Am. J. Cardiol. 11: 150–157, 1963.
 374. Permutt, S., B. Bromberger‐Barnea, And H. N. Bane. Alveolar pressure, pulmonary venous pressure and the vascular waterfall. Med. Thorac. 19: 239–260, 1962.
 375. Permutt, S., P. Caldini, A. Maseri, W. H. Palmer, T. Sasamori, And K. Zierler. Recruitment versus distensibility in the pulmonary vascular bed. In: Pulmonary Circulation and Interstitial Space, edited by A. P. Fishman and H. H. Hecht. Chicago, IL: Univ. of Chicago Press, 1969, p. 375–387.
 376. Permutt, S., J. B. L. Howell, D. F. Proctor, And R. L. Riley. Effect of lung inflation on static pressure‐volume characteristics of pulmonary vessels. J. Appl. Physiol. 16: 64–70, 1961.
 377. Peroutka, S. J., and S. H. Snyder. Multiple serotonin receptors: differential binding of [3H]5‐hydroxytryptamine, [3H]lysergic acid diethylamide and [3H]spiroperidol. Mol. Pharmacol. 16: 687–699, 1979.
 378. Perrault, J. L., J. Morinet, F. A. Nader, And A. Lockhart. Influence de l'age et de l'exercice physique sur les pressions dans la circulation pulmonaire de sujects normaux ages de plus de quarante ans. Bull. Physio‐Pathol. Respir. 5: 505–522, 1969.
 379. Peterson, J. W., and R. J. Paul. Aerobic glycolysis in vascular smooth muscle: relation to isometric tension. Biochim. Biophys. Acta 357: 167–176, 1974.
 380. Petrini, M. F., B. T. Peterson, And R. W. Hyde. Lung tissue volume and blood flow by rebreathing: theory. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 795–802, 1978.
 381. Piene, H. The influence of pulmonary blood flow rate on vascular input impedance and hydraulic power in the sympathetically and noradrenaline stimulated cat lung. Acta Physiol. Scand. 98: 44–53, 1976.
 382. Piene, H. Influence of vessel distension and myogenic tone on pulmonary arterial input impedance. A study using a computer model of rabbit lung. Acta Physiol. Scand. 98: 54–66, 1976.
 383. Piene, H. and T. Sund. Flow and power output of right ventricle facing load with variable input impedance. J. Appl. Physiol. 237 (Heart Circ. Physiol. 6): H125–H130, 1979.
 384. Pietra, G. G., M. Magno, L. Johns, And A. P. Fishman. Bronchial veins and pulmonary edema. In: Pulmonary Edema, edited by A. P. Fishman and E. M. Renkin. Bethesda, MD: Am. Physiol. Soc, 1979, p. 195–206.
 385. Pietra, G. G., J. P. Szidon, M. M. Leventhal, And A. P. Fishman. Histamine and interstitial pulmonary edema in the dog. Circ. Res. 29: 323–337, 1971.
 386. Piiper, J. Grosse des Arterien‐, des Capillar‐ und des Venenvolumens in der isolierten Hundelunge. Pfluegers Arch. Gesamte Physiol. Menschen Tiere 269: 182–193, 1959.
 387. Pinsky, M. R., W. R. Summer, R. A. Wise, S. Permutt, And B. Bromberger‐Barnea. Augmentation of cardiac function by elevation of intrathoracic pressure. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 950–955, 1983.
 388. Pirlo, A. F., J. L. Benumof, And F. R. Trousdale. Atelectatic lobe blood flow: open vs. closed chest, positive pressure vs. spontaneous ventilation. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 50: 1022–1026, 1981.
 389. Porcelli, R. J., and E. H. Bergofsky. Adrenergic receptors in pulmonary vasoconstrictor responses to gaseous and humoral agents. J. Appl. Physiol. 34: 483–488, 1973.
 390. Pouleur, H., J. Lefevre, C. Van Eyll, P. M. Jaumin, And A. A. Charlier. Significance of pulmonary input impedance in right ventricular performance. Cardiovasc. Res. 12: 617–629, 1978.
 391. Quebbeman, E. J., and C. A. Dawson. Influence of inflation and atelectasis on the hypoxic pressor response in isolated dog lung lobes. Cardiovasc. Res. 10: 672–677, 1976.
 392. Qvist, J., H. Pontoppidan, R. S. Wilson, E. Lowenstein, And M. B. Laver. Hemodynamic responses to mechanical ventilation with PEEP. Anesthesiology 42: 45–55, 1975.
 393. Rabinovitch, M., W. J. Gamble, O. S. Miettinen, And L. Reid. Age and sex influence on pulmonary hypertension of chronic hypoxia and on recovery. Am. J. Physiol. 240 (Heart Circ. Physiol. 9): H62–H72, 1981.
 394. Rabinovitch, M., W. Gamble, A. S. Nadas, O. S. Miettinen, And L. Reid. Rat pulmonary circulation after chronic hypoxia: hemodynamic and structural features. Am. J. Physiol. 236 (Heart Circ. Physiol. 5): H818–H827, 1979.
 395. Rabinovitch, M., M. A. Konstam, W. J. Gamble, N. Papanicolau, S. Treves, And L. Reid. Changes in pulmonary blood flow affect vascular response to chronic hypoxia in rat. Circ. Res. 52: 432–441, 1983.
 396. Rajagopalan, B., C. D. Bertram, T. Stallard, And G. de J. Lee. Blood flow in pulmonary veins. III. Simultaneous measurements of their dimensions, intravascular pressure and flow. Cardiovasc. Res. 13: 684–692, 1979.
 397. Reeves, J. T., R. F. Grover, G. F. Filley, And S. G. Blount Jr.. Circulatory changes in man during mild supine exercise. J. Appl. Physiol. 16: 279–282, 1961.
 398. Reeves, J. T., and B. M. Groves. Approach to the patient with pulmonary hypertension. In: Pulmonary Hypertension, edited by E. K. Weir and J. T. Reeves. Mount Kisco, NY: Futura, 1984, p. 1–44.
 399. Reeves, J. T., P. Jokl, J. Merida, And J. E. Leathers. Pulmonary vascular obstruction following administration of high‐energy nucleotides. J. Appl. Physiol. 22: 475–479, 1967.
 400. Reeves, J. T., W. W. Wagner, Jr., I. F. McMurtry, And R. F. Grover. Physiological effects of high altitude on the pulmonary circulation. In: Environmental Physiology III, edited by D. Robertshaw. Baltimore, MD: University Park, 1979, vol. 20, p. 289–310. (Int. Rev. Physiol. Ser.)
 401. Regoli, D., J. Mizrahi, P. D'Orleans‐Juste, And S. Caranikas. Effects of kinins on isolated blood vessels. Role of endothelium. Can. J. Physiol. Pharmacol. 60: 1580–1583, 1982.
 402. Reid, L. M. The pulmonary circulation remodeling in growth and disease. Am. Rev. Respir. Dis. 119: 531–546, 1979.
 403. Reid, L. and B. Meyrick. Hypoxia and pulmonary vascular endothelium. In: Metabolic Activities of the Lung. Amsterdam: Excerpta Med., 1980, p. 37–60. (Ciba Found. Symp. 78.)
 404. Remy, J., A. Arnaud, H. Fardou, R. Giraud, And C. Voisin. Treatment of hemoptysis by embolization of bronchial arteries. Radiology 122: 33–37, 1977.
 405. Reuben, S. R. Wave transmission in the pulmonary arterial system in disease in man. Circ. Res. 27: 523–529, 1970.
 406. Reuben, S. R. Compliance of the human pulmonary arterial system in disease. Circ. Res. 29: 40–50, 1971.
 407. Reuben, S. R., B. J. Gersh, J. P. Swadling, And G. de J. Lee. Measurement of pulmonary arterial distensibility. Cardiovasc. Res. 4: 473–481, 1970.
 408. Reuben, S. R., J. P. Swadling, B. J. Gersh, And G. de J. Lee. Impedance and transmission properties of the pulmonary arterial system. Cardiovasc. Res. 5: 1–9, 1971.
 409. Rickaby, D. A., C. A. Dawson, And M. B. Maron. Pulmonary inactivation of serotonin and site of serotonin pulmonary vasoconstriction. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 48: 606–612, 1980.
 410. Rickaby, D. A., J. H. Linehan, T. A. Bronikowski, And C. A. Dawson. Kinetics of serotonin uptake in the dog lung. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 405–414, 1981.
 411. Riley, R. L. Effect of lung inflation upon the pulmonary vascular bed. In: Pulmonary Structure and Function, edited by A. V. S. de Reuck and M. O'Connor. Boston, MA: Little, Brown, 1962, p. 261–272. (Ciba Found. Symp.)
 412. Robotham, J. L., W. Lixfeld, L. Holland, D. MacGregor, B. Bromberger‐Barnea, S. Permutt, And J. L. Rabson. The effects of positive end‐expiratory pressure on right and left ventricular performance. Am. Rev. Respir. Dis. 121: 677–683, 1980.
 413. Rodbard, S. and H. Murao. Ventilatory effects on pulmonary vascular inflow and outflow patterns. Cardiovasc. Res. 11: 177–186, 1977.
 414. Roos, S. D., E. K. Weir, And J. T. Reeves. Meclofenamate does not reduce chronic hypoxic pulmonary vasoconstriction. Experientia 32: 195–196, 1976.
 415. Rorie, D. K., and G. M. Tyce. Effects of hypoxia on norepinephrine release and metabolism in dog pulmonary artery. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 750–758, 1983.
 416. Rose, C. E., Jr., J. A. Althaus, D. L. Kaiser, E. D. Miller, And R. M. Carey. Acute hypoxemia and hypercapnia: increase in plasma catecholamines in conscious dogs. Am. J. Physiol. 245 (Heart Circ. Physiol. 14): H924–H929, 1983.
 417. Rosenzweig, D. Y., J. M. B. Hughes, And J. B. Glazier. Effects of transpulmonary and vascular pressures on pulmonary blood volume in isolated lung. J. Appl. Physiol. 28: 553–560, 1970.
 418. Rotta, A., A. Cánepa, A. Hurtado, T. Velásquez, And R. Chavez. Pulmonary circulation at sea level and at high altitudes. J. Appl. Physiol. 9: 328–336, 1956.
 419. Rounds, S., and I. F. McMurtry. Inhibitors of oxidative ATP production cause transient vasoconstriction and block subsequent pressor responses in rat lungs. Circ. Res. 48: 393–400, 1981.
 420. Rounds, S., I. F. McMurtry, And J. T. Reeves. Glucose metabolism accelerates the decline of hypoxic vasoconstriction in rat lungs. Respir. Physiol. 44: 239–249, 1981.
 421. Rubin, L. J., and J. D. Lazar. Influence of prostaglandin synthesis inhibitors on pulmonary vasodilatory effects of hydralazine in dogs with hypoxic pulmonary vasoconstriction. J. Clin. Invest. 67: 193–200, 1981.
 422. Rubin, L. J., and J. D. Lazar. Nonadrenergic effects of isoproterenol in dogs with hypoxic pulmonary vasoconstriction. Possible role of prostaglandins. J. Clin. Invest. 71: 1366–1374, 1983.
 423. Rudolph, A. M. Fetal and neonatal pulmonary circulation. Am. Rev. Respir. Dis. 115: 11–18, 1977.
 424. Rudolph, A. M. Fetal and neonatal pulmonary circulation. Annu. Rev. Physiol. 41: 383–395, 1979.
 425. Rudolph, A. M., P. A. M. Auld, R. J. Golinko, And M. H. Paul. Pulmonary vascular adjustments in the neonatal period. Pediatrics 28: 28–34, 1961.
 426. Rudolph, A. M., M. A. Heymann, And A. B. Lewis. Physiology and pharmacology of the pulmonary circulation in the fetus and newborn. In: Lung Biology in Health and Disease. Development of the Lung, edited by W. A. Hodson. New York: Dekker, 1977, vol. 6, chapt. 14, p. 497–523.
 427. Rudolph, A. M. and S. Yuan. Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes. J. Clin. Invest. 45: 399–411, 1966.
 428. Ruiz, A. V., G. E. Bisgard, And J. A. Will. Hemodynamic responses to hypoxia and hyperoxia in calves at sea level and altitude. Pfluegers Arch. 344: 275–286, 1973.
 429. Ryan, K., P. Kvietys, J. C. Parker, And A. E. Taylor. Comparison of venous occlusion and isogravimetric capillary pressures in isolated dog lungs (Abstract). Physiologist 23: 76, 1980.
 430. Said, S. I. Pulmonary metabolism of prostaglandins and vasoactive peptides. Annu. Rev. Physiol. 44: 257–268, 1982.
 431. Said, S. I. Vasodilator action of VIP: introduction and general considerations. In: Vasoactive Intestinal Peptide, edited by S. I. Said. New York: Raven, 1982, p. 145–148.
 432. Said, S. I., T. Yoshida, S. Kitamura, And C. Vreim. Pulmonary alveolar hypoxia: release of prostaglandins and other humoral mediators. Science 185: 1181–1183, 1974.
 433. Saldana, M. E., R. A. Harley, A. A. Liebow, And C. B. Carrington. Experimental extreme pulmonary hypertension and vascular disease in relation to polycythemia. Am. J. Pathol. 52: 935–981, 1968.
 434. Salisbury, P. F., P. Weil, And D. State. Factors influencing collateral blood flow to the dog's lung. Circ. Res. 5: 303–309, 1957.
 435. Samuelsson, B. Leukotrienes: mediators of immediate hypersensitivity reactions and inflammation. Science 220: 568–575, 1983.
 436. Shaw, J. W. Pulmonary vasodilator and vasoconstrictor actions of histamine (Abstract). J. Physiol. London 215: 34P–35P, 1971.
 437. Shelub, I., A. Van Grondelle, R. McCullough, S. Hofmeister, And J. T. Reeves. A model of embolic chronic pulmonary hypertension in the dog. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 56: 810–815, 1984.
 438. Shettigar, U. R., H. N. Hultgren, M. Specter, R. Martin, And D. H. Davies. Primary pulmonary hypertension: favorable effect of isoproterenol. N. Engl. J. Med. 295: 1414–1415, 1976.
 439. Shoukas, A. S. Pressure‐flow and pressure‐volume relations in the entire pulmonary vascular bed of the dog determined by two‐part analysis. Circ. Res. 37: 809–818, 1975.
 440. Siegelman, S. S., J. W. C. Hagstrom, S. K. Koerner, And F. J. Veith. Restoration of bronchial artery circulation after canine lung allotransplantation. J. Thorac. Cardiovasc. Surg. 73: 792–795, 1977.
 441. Silove, E. D., and R. F. Grover. Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular responses to hypoxia. J. Clin. Invest. 47: 274–285, 1968.
 442. Silove, E. D., T. Inoue, And R. F. Grover. Comparison of hypoxia, pH, and sympathomimetic drugs on bovine pulmonary vasculature. J. Appl. Physiol. 24: 355–365, 1968.
 443. Singhal, S., R. Henderson, K. Horsfeld, K. Harding, And G. Cumming. Morphometry of the human pulmonary arterial tree. Circ. Res. 33: 190–197, 1973.
 444. Skalak, R., F. Wiener, E. Morkin, And A. P. Fishman. The energy distribution in the pulmonary circulation. II. Experiments. Phys. Med. Biol. 11: 437–449, 1966.
 445. Smith, H. C. and J. Butler. Pulmonary venous waterfall and perivenous pressure in the living dog. J. Appl. Physiol. 38: 304–308, 1975.
 446. Smith, P. and D. Heath. Ultrastructure of hypoxic hypertensive pulmonary vascular disease. J. Pathol. 121: 93–100, 1977.
 447. Smith, P., H. Moosavi, M. Winson, And D. Heath. The influence of age and sex on the response of the right ventricle, pulmonary vasculature and carotid bodies to hypoxia in rats. J. Pathol. 112: 11–18, 1974.
 448. Snapper, J. R., A. A. Hutchison, M. L. Ogletree, And K. L. Brigham. Effects of cyclooxygenase inhibitors on the alterations in lung mechanics caused by endotoxemia in the unanesthetized sheep. J. Clin. Invest. 72: 63–76, 1983.
 449. Sobin, S. S., H. M. Tremer, And Y. C. Fung. Morphometric basis of the sheet‐flow concept of the pulmonary alveolar microcirculation in the cat. Circ. Res. 26: 397–414, 1970.
 450. Sobin, S. S., H. M. Tremer, J. D. Hardy, And H. P. Chiodi. Changes in arteriole in acute and chronic hypoxic pulmonary hypertension and recovery in rat. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 1445–1455, 1983.
 451. Somlyo, A. P., and A. V. Somlyo. Vascular smooth muscle. II. Pharmacology of normal and hypertensive vessels. Pharmacol. Rev. 22: 249–353, 1970.
 452. Souhrada, J. F., D. W. Dickey, And R. A. Schultz. The role of substrate in the hypoxic response of the pulmonary artery. Chest 71: 252–253, 1977.
 453. Spannhake, E. W., A. L. Hyman, And P. J. Kadowitz. Dependence of the airway and pulmonary vascular effects of arachidonic acid upon route and rate of administration. J. Pharmacol. Exp. Ther. 212: 584–590, 1980.
 454. Spencer, H. and D. Leof. The innervation of the human lung. J. Anat. 98: 559–609, 1964.
 455. Spiro, S. G., B. H. Culver, And J. Butler. Pressure outside the extrapulmonary airway in dogs. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 45: 437–441, 1978.
 456. Sprague, R. S., A. H. Stephenson, L. J. Heitmann, And A. J. Lonigro. Differential response of the pulmonary circulation to PGE2 and PGF2‐α. in the presence of unilateral alveolar hypoxia (Abstract). Clin. Res. 30: A784, 1982.
 457. Stalcup, S. A., P. J. Leuenberger, J. S. Lipset, M. M. Osman, J. M. Cerreta, R. B. Mellins, And G. M. Turino. Impaired angiotensin conversion and bradykinin clearance in experimental canine pulmonary emphysema. J. Clin. Invest. 67: 201–209, 1981.
 458. Stanbrook, H. S., and I. F. McMurtry. Inhibition of glycolysis potentiates hypoxic vasoconstriction in rat lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 1467–1473, 1983.
 459. Stern, S., R. E. Ferguson, And E. Rapaport. Reflex pulmonary vasoconstriction due to stimulation of the aortic body by nicotine. Am. J. Physiol. 206: 1189–1195, 1964.
 460. Stocks, J., K. Costeloe, C. P. Winlove, And S. Godfrey. Measurement of pulmonary capillary blood flow in infants by plethysmography. J. Clin. Invest. 59: 490–499, 1977.
 461. Strawbridge, H. T. G. Chronic pulmonary emphysema. An experimental study. Am. J. Pathol. 37: 161–174, 1960.
 462. Su, C., and J. A. Bevan. Pharmacology of pulmonary blood vessels. Pharmacol. Ther. B 2: 275–288, 1976.
 463. Susmano, A., and R. A. Carleton. Prevention of hypoxic pulmonary hypertension by chlorpheniramine. J. Appl. Physiol. 31: 531–535, 1971.
 464. Suzuki, H., and B. M. Twarog. Membrane properties of smooth muscle cells in pulmonary arteries of the rat. Am. J. Physiol. 242 (Heart Circ. Physiol. 11): H900–H906, 1982.
 465. Suzuki, H., and B. M. Twarog. Membrane properties of smooth muscle cells in pulmonary hypertensive rats. Am. J. Physiol. 242 (Heart Circ. Physiol. 11): H907–H915, 1982.
 466. Svanberg, L. Influence of posture on the lung volumes, ventilation and circulation in normals. Scand. J. Clin. Lab. Invest. Suppl. 25: 1–95, 1957.
 467. Sylvester, J. T., A. L. Harabin, M. D. Peake, And R. S. Frank. Vasodilator and constrictor responses to hypoxia in isolated pig lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 49: 820–825, 1980.
 468. Sylvester, J. T. and C. McGowan. The effects of agents that bind to cytochrome P‐450 on hypoxic pulmonary vasoconstriction. Circ. Res. 43: 429–437, 1978.
 469. Sylvester, J. T., W. Mitzner, Y. Ngeow, And S. Permutt. Hypoxic constriction of alveolar and extra‐alveolar vessels in isolated pig lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 1660–1666, 1983.
 470. Sylvester, J. T., S. M. Scharf, R. D. Gilbert, R. S. Fitzgerald, And R. J. Traystman. Hypoxic and CO hypoxia in dogs: hemodynamics, carotid reflexes, and catecholamines. Am. J. Physiol. 236 (Heart Circ. Physiol. 5): H22–H28, 1979.
 471. Szidon, J. P., and A. P. Fishman. Autonomic control of the pulmonary circulation. In: Pulmonary Circulation and Interstitial Space, edited by A. P. Fishman and H. H. Hecht. Chicago, IL: Univ. of Chicago Press, 1969, p. 239–268.
 472. Szidon, J. P., and A. P. Fishman. Participation of pulmonary circulation in the defense reaction. Am. J. Physiol. 220: 364–370, 1971.
 473. Szidon, J. P., and J. F. Flint. Significance of sympathetic innervation of pulmonary vessels in response to acute hypoxia. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 65–71, 1977.
 474. Taylor, C. R., and E. R. Weibel. Design of the mammalian respiratory system. I. Problems and strategy. Respir. Physiol. 44: 1–10, 1981.
 475. Tenney, S. M. A comparative survey of the design of respiratory systems for gas exchange. In: Pulmonary Diseases and Disorders, edited by A. P. Fishman. New York: McGraw‐Hill, 1980, p. 282–297.
 476. Thilenius, O. G., B. M. Candiolo, And J. L. Beug. Effect of adrenergic blockade on hypoxia‐induced pulmonary vasoconstriction in awake dogs. Am. J. Physiol. 213: 990–998, 1967.
 477. Thilenius, O. G. and C. Derenzo. Effects of acutely induced changes in arterial pH on pulmonary vascular resistance during normoxia and hypoxia in awake dogs. Clin. Sci. 42: 277–287, 1972.
 478. Thomas, H. M., III, and R. C. Garrett. Strength of hypoxic vasoconstriction determines shunt fraction in dogs with atelectasis. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 53: 44–51, 1982.
 479. Thompson, B., G. R. Barer, And J. W. Shaw. The action of histamine on pulmonary vessels of cats and rats. Clin. Exp. Pharmacol. Physiol. 3: 399–414, 1976.
 480. Thompson, J. H. Serotonin and the alimentary tract. Res. Commun. Chem. Pathol. Pharmacol. 2: 687–781, 1981.
 481. Todd, T. R., E. M. Baile, And J. C. Hogg. Pulmonary arterial wedge pressure in hemorrhagic shock. Am. Rev. Respir. Dis. 118: 613–616, 1978.
 482. Tooker, J., J. Huseby, And J. Butler. The effect of Swan‐Ganz catheter height on the wedge pressure‐left atrial pressure relationships in edema during positive‐pressure ventilation. Am. Rev. Respir. Dis. 117: 721–725, 1978.
 483. Torrance, R. W. The idea of a chemoreceptor. In: Pulmonary Circulation and Interstitial Space, edited by A. P. Fishman and H. H. Hecht. Chicago, IL: Univ. of Chicago Press, 1969, p. 223–237.
 484. Tucker, A., I. F. McMurtry, A. F. Alexander, J. T. Reeves, And R. F. Grover. Lung mast cell density and distribution in chronically hypoxic animals. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 174–178, 1977.
 485. Tucker, A., I. F. McMurtry, J. T. Reeves, A. F. Alexander, D. H. Will, And R. F. Grover. Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude. Am. J. Physiol. 228: 762–767, 1975.
 486. Tucker, A., E. K. Weir, J. T. Reeves, And R. F. Grover. Histamine H1‐ and H2‐receptors in pulmonary and systemic vasculature of the dog. Am. J. Physiol. 229: 1008–1013, 1975.
 487. Tucker, A., E. K. Weir, J. T. Reeves, And R. F. Grover. Failure of histamine antagonists to prevent hypoxic pulmonary vasoconstriction in dogs. J. Appl. Physiol. 40: 496–500, 1976.
 488. Turlapaty, P. D. M. V., and B. M. Altura. Extracellular magnesium ions control calcium exchange and content of vascular smooth muscle. Eur. J. Pharmacol. 52: 421–423, 1978.
 489. Turner, J. H., and J. J. Lalich. Experimental cor pulmonale in the rat. Arch. Pathol. 79: 409–418, 1965.
 490. Tyler, T., R. Wallis, C. Leffler, And S. Cassin. The effects of indomethacin on the pulmonary vascular response to hypoxia in the premature and mature newborn goat. Proc. Soc. Exp. Biol. Med. 150: 695–698, 1975.
 491. Unger, M., M. Atkins, W. A. Briscoe, And T. K. C. King. Potentiation of pulmonary vasoconstrictor response with repeated intermittent hypoxia. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 662–667, 1977.
 492. Vaage, J., L. Bjetnaes, And A. Hauge. The pulmonary vasoconstrictor response to hypoxia: effects of inhibitors of prostaglandin biosynthesis. Acta Physiol. Scand. 95: 95–101, 1975.
 493. Vaage, J. and A. Hauge. Prostaglandins and the pulmonary vasoconstrictor response to alveolar hypoxia. Science 189: 899–900, 1975.
 494. Valdivia, E., Y. Hayashi, J. J. Lalich, And J. Sonnad. Capillary obstruction in experimental cor pulmonale (Abstract). Circulation Suppl. 32: 211, 1965.
 495. Van Den Bos, G. C., N. Westerhof, And O. S. Randall. Pulse wave reflection: can it explain the differences between systemic and pulmonary pressure and flow waves? Circ. Res. 51: 479–485, 1982.
 496. Vane, J. R. Clinical potential of prostacyclin. In: Advances in Prostaglandin, Thromboxane and Leukotriene Research, edited by B. Samuelsson, R. Paoletti, and P. Ramwell. New York: Raven, 1982, vol. 11, p. 449–461.
 497. Vane, J. R. Prostacyclin (Editorial). J. R. Soc. Med. 76: 245–249, 1983.
 498. Van Neuten, J. H., J. E. Leysen, J. A. J. Sohuurkes, And P. M. Vanhoutte. Ketanserum, a selective antagonist of 5‐HT2 serotonergic receptors. Lancet 1: 297–298, 1983.
 499. Vermeire, P. and J. Butler. Effect of respiration on pulmonary capillary blood flow in man. Circ. Res. 22: 299–303, 1968.
 500. Voelkel, N. F., J. G. Gerber, I. F. McMurtry, A. S. Nies, And J. T. Reeves. Release of vasodilator prostaglandin, PGI2, from isolated rat lung during vasoconstriction. Circ. Res. 48: 207–213, 1981.
 501. Voelkel, N. F., I. McMurtry, And J. Reeves. High extracellular calcium causes pulmonary vasodilation by stimulating Na + K + ATPase. Symposium on the mechanism of vasodilation (Abstract). Blood Vessels 17: 168, 1980.
 502. Voelkel, N. F., R. D. Olson, I. F. McMurtry, And J. T. Reeves. Vanadate potentiates hypoxic pulmonary vasoconstriction (Abstract). Federation Proc. 39: 766, 1980.
 503. Vogel, J. H. K., W. F. Weaver, R. L. Rose, S. G. Blount, And R. F. Grover. Pulmonary hypertension and exertion in normal man living at 10,150 feet. Med. Thorac. 19: 461–477, 1962.
 504. Vreim, C. E., and N. C. Staub. Indirect and direct pulmonary capillary blood volume in anesthetized open‐thorax cats. J. Appl. Physiol. 34: 452–459, 1973.
 505. Vreim, C. E., and N. C. Staub. Pulmonary vascular pressures and capillary blood volume changes in anesthetized cats. J. Appl. Physiol. 36: 275–279, 1974.
 506. Vuori, A. Central hemodynamics, oxygen transport and oxygen consumption during three methods for CPAP. Acta Anaesthesiol. Scand. 25: 376–380, 1981.
 507. Wagenvoort, C. A. and N. Wagenvoort. Pathology of Pulmonary Hypertension. New York: Wiley, 1977, 345 p.
 508. Wagner, W. W., Jr., And L. P. Latham. Vasomotion in the pulmonary microcirculation. In: Small Vessel Angiography. Imaging, Morphology, Physiology, and Clinical Applications, edited by B. K. Hilal and S. Baum. St. Louis, MO: Mosby, 1973, p. 301–306. (Symp. Radiological Res., 3rd, Glen Cove, NY, 1972.)
 509. Wagner, W. W., Jr., L. P. Latham, M. N. Gillespie, And J. P. Guenther. Direct measurement of pulmonary capillary transit times. Science 218: 379–381, 1982.
 510. Walcott, G., H. B. Burchell, And A. L. Brown. Primary pulmonary hypertension. Am. J. Med. 49: 70–79, 1970.
 511. Wanner, A., R. Begin, M. Cohn, And M. A. Sackner. Vascular volumes of the pulmonary circulation in intact dogs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 956–963, 1978.
 512. Warrell, D. A., J. W. Evans, R. O. Clarke, G. P. Kingaby, And J. B. West. Pattern of filling in the pulmonary capillary bed. J. Appl. Physiol. 32: 346–356, 1972.
 513. Weibel, E. R. Morphometry of the Human Lung. Heidelberg: Springer‐Verlag, 1963.
 514. Weibel, E. R. On pericytes, particularly their existence on lung capillaries. Microvasc. Res. 8: 218–235, 1974.
 515. Weibel, E. R. Design and structure of the human lung. In: Pulmonary Diseases and Disorders, edited by A. P. Fishman. New York: McGraw‐Hill, 1980. p. 224–271.
 516. Weibel, E. R. and J. Gil. Structure‐function relationships at the alveolar level. In: Lung Biology in Health and Disease. Bioengineering Aspects of the Lung, edited by J. B. West. New York: Dekker, 1977, vol. 3, chapt. 1, p. 1–81.
 517. Weir, E. K., I. F. McMurtry, A. Tucker, J. T. Reeves, And R. F. Grover. Prostaglandin synthetase inhibitors do not decrease hypoxic pulmonary vasoconstriction. J. Appl. Physiol. 41: 714–718, 1976.
 518. Weir, E. K., J. T. Reeves, And R. F. Grover. Prostaglandin E1 inhibits the pulmonary vascular pressor response to hypoxia and prostaglandin F2‐α. Prostaglandins 10: 623–631, 1975.
 519. Weir, E. K., A. Tucker, J. T. Reeves, D. H. Will, And R. F. Grover. The genetic factor influencing pulmonary hypertension in cattle at high altitude. Cardiovasc. Res. 8: 745–749, 1974.
 520. Weir, E. K., D. H. Will, A. F. Alexander, I. F. McMurtry, R. Looga, J. T. Reeves, And R. F. Grover. Vascular hypertrophy in cattle susceptible to hypoxic pulmonary hypertension. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 517–521, 1979.
 521. Weiskopf, R. B., and J. W. Severinghaus. Diffusing capacity of the lung for CO in man during acute acclimation to 14,246 ft. J. Appl. Physiol. 32: 285–289, 1972.
 522. West, J. B. Regional Differences in the Lung. New York: Academic, 1977, p. 85–165.
 523. West, J. B., and C. T. Dollery. Distribution of blood flow and the pressure‐flow relations of the whole lung. J. Appl. Physiol. 20: 175–183, 1965.
 524. West, J. B., C. T. Dollery, And A. Naimark. Distribution of blood flow in isolated lung: relation to vascular and alveolar pressures. J. Appl. Physiol. 19: 713–724, 1964.
 525. West, J. B., A. M. Schneider, And M. M. Mitchell. Recruitment in networks of pulmonary capillaries. J. Appl. Physiol. 39: 976–984, 1975.
 526. Wetzel, R. C., and J. T. Sylvester. Gender differences in hypoxic vascular response of isolated sheep lungs. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 100–104, 1983.
 527. Wiener, F., E. Morkin, R. Skalak, And A. P. Fishman. Wave propagation in the pulmonary circulation. Circ. Res. 19: 834–850, 1966.
 528. Will, D. H., I. F. McMurtry, J. T. Reeves, And R. F. Grover. Cold‐induced pulmonary hypertension in cattle. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 469–473, 1978.
 529. Williams, A., D. Heath, P. Harris, D. Williams, And P. Smith. Pulmonary mast cells in cattle and llamas at high altitude. J. Pathol. 134: 1–16, 1981.
 530. Woods, J. R., Jr., C. R. Brinkman III, A. Dandavino, K. Murayama, And N. S. Assali. Action of histamine and H1 and H2 blockers on the cardiopulmonary circulation. Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H73–H78, 1977.
 531. Yokochi, K., P. M. Olley, E. Sideis, F. Hamilton, D. Huhtaner, And F. Coceani. Leukotriene D4: a potent vasoconstrictor of the pulmonary and systemic circulations in the newborn lamb. In: Advances in Prostaglandin, Thromboxane and Leukotriene Research, edited by B. Samuelsson and R. Paoletti. New York: Raven, 1981, vol. 11, p. 211–214.
 532. Yu, P. N. Pulmonary Blood Volume in Health and Disease. Philadelphia, PA: Lea & Febiger, 1969.
 533. Zapol, W. M., and M. T. Snider. Pulmonary hypertension in severe acute respiratory failure. N. Engl. J. Med. 296: 476–480, 1977.
 534. Zasslow, M. A., J. L. Benumof, And F. R. Trousdale. Hypoxic pulmonary vasoconstriction and the size of hypoxic compartment. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 626–630, 1982.
 535. Zhu, Y. J., R. Kradin, R. D. Brandstetter, G. Staton, J. Moss, and C. A. Hales. Hypoxic pulmonary hypertension in the mast cell‐deficient mouse. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 680–686, 1983.
 536. Zhuang, F. Y., Y. C. Fung, And R. T. Yen. Analysis of blood flow in cat's lung with detailed anatomical and elasticity data. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55: 1341–1348, 1983.
 537. Zucker, M. B. The platelet release reactions. In: Platelets, Drugs, and Thrombosis, edited by J. Hirsch, J. F. Cade, A. S. Gallus, and E. Schonbaum. Basel: Karger, 1975, p. 27–34.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

How to Cite

Alfred P. Fishman. Pulmonary Circulation. Compr Physiol 2011, Supplement 10: Handbook of Physiology, The Respiratory System, Circulation and Nonrespiratory Functions: 93-165. First published in print 1985. doi: 10.1002/cphy.cp030103