Comprehensive Physiology Wiley Online Library

Vertebrate Respiratory Gas Exchange

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Abstract

The sections in this article are:

1 General Model: Symbols and Basic Equations
2 External Medium: Water vs. Air Breathing
2.1 Respiratory Gas Transfer
2.2 Consequences Arising from Other Physical Properties of Water
3 Internal Medium: Blood
3.1 Oxygen Transport
3.2 Carbon Dioxide Transport
4 Four Models for Vertebrate Gas Exchange Organs
4.1 Structural Design
4.2 Models for Gas Exchange
5 Medium/Blood Diffusion Limitation in the Gas Exchange Models
5.1 Diffusion and Perfusion in Alveolar Lungs
5.2 Diffusing Capacity
5.3 Cutaneous Gas Exchange in Amphibia
5.4 Parabronchial Gas Exchange at High Altitude
6 Limitations to the Applicability of the Models
6.1 Unsteady State
6.2 Medium Flow and Composition: Dead Space
6.3 Blood Flow and Composition: Vascular Shunt
6.4 Other Problems
7 Diffusion in the Respired Medium
7.1 Diffusion Limitation in the Alveolar Space of Mammalian Lungs
7.2 Stratification in Air Capillaries of Bird Lungs
7.3 Stratification in Skin Breathing
7.4 Diffusion Limitation in the Interlamellar Water of Fish Gills
8 Ventilation, Diffusion, and Perfusion
8.1 Various Models
8.2 Diffusion‐Limited Counter‐current Exchange in Fish Gills
9 Unequal Distribution of Ventilation to Perfusion
9.1 Conventional Three‐Compartment Lung Model
9.2 Detection of Continuous Distributions of V.AtoQ.
9.3 Ventilation–Perfusion Heterogeneity in Nonmammalian Vertebrates
10 Unequal Distribution of Diffusing Capacity
10.1 Inequality of the Equilibration Coefficient
10.2 Unequal Distribution of Gas‐Phase Conductance
11 Special Adaptation: Fish Swimbladder
11.1 Swimbladder Architecture
11.2 Swimbladder Gas
11.3 Mechanisms for Deposition of Gas: The Classical Model
11.4 Additions to the Classical Model
Figure 1. Figure 1.

Illustration of the more important symbols used in this article. (A) Generalized symbols, used for modeling, fish gills, and bird lungs. , ventilation (air or water); , blood flow (perfusion); P1, Pe, Pv, Pa, partial pressures in inspired (i) and expired (e) media and in mixed venous (v) and arterialized (a) blood. (B) Mammalian symbols, used for mammalian lungs. e, total expired ventilation; d, dead space ventilation; a, alveolar ventilation; c, pulmonary capillary blood flow; sh, shunt blood flow; , total pulmonary blood flow; P, partial pressures in inspired gas (i), alveolar gas (a), end‐expired gas (e′), (mixed) expired gas (e); in mixed venous blood ( ) and arterial blood (a). (After ref. ).

Figure 2. Figure 2.

Partial pressure–concentration relationships of O2 and CO2 in air (left) and in seawater (containing bicarbonate/carbonate, right). CO2 in water refers to “total” CO2 (physically dissolved CO2, bicarbonate, and carbonate). The slope of the lines is the capacitance coefficient β.

Figure 3. Figure 3.

The CO2–O2 diagram for transport of respiratory gases by convection (of air or water) or diffusion (in air, water, or tissue), RQ being 0.9. The identity line (ΔPCO2: ΔPO2 = 1.0) is attained for convective transport in air at RQ = 1.0. Ranges for partial pressures of CO2 and O2 observed in arterialized blood of air breathers and water breathers are indicated by shaded areas. Dual (bimodal/trimodal) breathers are located in the intermediate range indicated by the double arrow. Note the different scales for PCO2 and PO2. (After ref. ).

Figure 4. Figure 4.

O2 dissociation curve and influencing parameters. In each graph, O2 content in blood (CO2) is on the ordinate, PO2 on the abscissa; a and v denote arterial and venous PO2. (A) O2 capacity is lower in blood with lower hemoglobin concentration. Dashed lines connect corresponding points of CO2 and PO2 in arterial and venous blood: slope is βb. (B) Cooperativity at the hemoglobin subunits results in higher βb compared with noncooperative binding (hyperbola—for example, in myoglobin). (C) Bohr effect results in effective dissociation curve that is steeper than that of the pH of either the arterial or the venous blood. (D) Moving the curve to the left or right, thereby changing P50 to P′50 or P″50, changes the slope βb between the given arterial PO2 and the venous PO2. (After ref. ).

Figure 5. Figure 5.

Schematic anatomy of the gill apparatus in teleost fish. (A) Gill arches covered by the operculum. (B) Section of a gill arch carrying filaments and secondary lamellae; direction of water flow shown by arrow. (C) Section of a filament with secondary lamellae; counter‐current flow of water and blood shown by arrows. (D) Cross section of two adjacent secondary lamellae and the interposed interlamellar water space. (After ref. ).

Figure 6. Figure 6.

Schematic anatomy of the respiratory apparatus in birds. (A) Lung and the air sacs. (B) Connections of the air sacs (AS) to the bronchial system; arrow indicates direction of air flow. (C) Section of the lung. (D) Section of periparabronchial tissue (para‐bronchial lumen on the left), showing the blood and air capillary networks. (After ref. ).

Figure 7. Figure 7.

Models for gas exchange organs in vertebrates and partial pressures in medium (water or air) and blood. Profiles in medium, between the entrance to (i) and the exit from (e) the organ, as well as in blood, between venous (v) and arterial (a) values, are indicated. (After ref. ).

Figure 8. Figure 8.

Partial pressures in medium (expired, Pe, or alveolar, Pa, respectively) and blood (arterialized or arterial, Pa) leaving the gas exchange area, relative to the medium (Pi and blood Pv) entering the gas exchange area, as functions of the ventilatory/perfusive conductance ratio, ( · βw)/( · βb), for three models (no diffusion limitation). In (B) and (C), the dotted line marks the curve for model (A) and the shaded area, the blood–gas overlap region, where the ratio (Pe – Pa)/(Pi – Pv) is negative. (After ref. ).

Figure 9. Figure 9.

Equivalence between the effects of conductance mismatch and shunt in the counter‐current system, assuming Pi = 100 and Pv = 60 units (no diffusion limitation). In (B), the ideal system with X = ( · βw)/( · βb) = 1. In (A, upper figure), mismatch is produced by doubling perfusive conductance, which leads to ( · βw)/( · βb) < 1 and lowers Pa to 80. The same effect is obtained when the extra blood flow is channeled through a blood shunt, whereby ideal matching conditions in the gas exchange compartment are restored (A, lower figure). In (C), a mismatch is created by doubling water flow conductance, whereby ( · βw)/( · βb) > 1 and Pc = 80. The same effect is produced by a water shunt. (After ref. ).

Figure 10. Figure 10.

Total conductance, Gtot, as function of diffusive conductance, D (A), and perfusive conductance, · βb (B). The limiting cases of pure perfusion and diffusion limitation are marked by broken lines. (After ref. ).

Figure 11. Figure 11.

Diffusion–perfusion limitation in alveolar–capillary transfer of various gases. Center: D/( · βb) ratio on logarithmic scale. Left: Perfusion and diffusion limitation areas are marked by different hatching; end of limitation area is taken at L = 0.05 (Table ). Right: Approximate location of inert and chemically bonded gases for alveolar–capillary transfer in normal human lungs in resting conditions. (After ref. ).

Figure 12. Figure 12.

Schematic representation of stratification. Density of stippling in lung models visualizes partial pressure (or concentration) of a gas (for example, CO2). The concentration profile of a gas with highest inspired value (for example, O2) is also shown. E′ denotes end‐expired gas. (After ref. ).

Figure 13. Figure 13.

Models to show the origin of alveolar‐arterial differnces for CO2 and O2 (AaD) in lungs with incomplete gas mixing in alveolar space. Gas‐blood diffusion is assumed to be nonlimiting. Density of stippling marks concentration of CO2. (A) Model with two compartments ventilated in series. AaD is due to the fact that end‐expired gas (A′) originates in the proximal compartment (1) only, whereas arterial blood is a mixture. (B) Like (A), but only the distal compartment (2) is perfused. An AaD arises because end‐expired gas (A′) is derived from the proximal compartment (1) and arterial blood from the distal compartment (2). (After ref. ).

Figure 14. Figure 14.

Simplified lung model for analysis of incomplete intra‐pulmonary gas mixing (stratification). In analogy to models (B) of Figs. and , the partial pressure difference (Pe′ – Pa) is due to finite Gmix and the difference Pa – Pa to finite D. (After ref. ).

Figure 15. Figure 15.

Partial pressure profiles of O2 in avian air capillary model. In spite of considerable fall of PO2 along the air capillary, arterial PO2 (Pa) is close to parabronchial PO2 (Ppb) because of the distal‐to‐proximal direction of capillary blood flow along the air capillary. The counter‐current‐like behavior is illustrated by the gas–blood PO2 overlap. (After ref. ).

Figure 16. Figure 16.

Fish gill model and characteristic measurements. (A) Model for a row of secondary lamellae on a gill filament. The spatial axes x, y, and z serve for orientation of the cross sections in the other quadrants. aff and eff are crosssectioned afferent and efferent arteries (both running in the x direction). (B) Cross section of the secondary lamellae parallel to the filament surface. (1) Length of the secondary lamella, (2b) width of the interlamellar water space. (C) Cross section of the secondary lamellae along the filament length. The secondary lamellae of adjacent filaments are shown by broken lines. (h) Height of the secondary lamella. (D) The trapezoidal lamella. (lo) Length of the base of the secondary lamella; γ, base‐to‐top tapering factor of the secondary lamella. (After ref. ).

Figure 17. Figure 17.

Water velocity and PO2 profiles in model for interlamellar space. PO, PO2 on plate surface; Pi, PO2 of inspired water; e, PO2 of mixed expired water. (A) Model showing parabolic velocity profiles (marked by hatching) for base, middle plane, and top. Three transverse sections (1, entry; 2, middle; 3, exit) are indicated. a and b refer to vertical sections in the y–z plane, in the middle and toward one side, respectively. (B) Longitudinal (y direction) PO2 profiles in planes a and b (at a fixed z value). (C) Vertical (z direction) PO2 profiles in planes 1, 2, and 3 (at a fixed x value). (D) Transverse (x direction) PO2 profiles in planes 1, 2, and 3 (at a fixed z value). (After ref. ).

Figure 18. Figure 18.

Inefficiency of O2 equilibration (ε) as a function of ϕ for selected values of tapering (γ). Stippled area: range of estimated γ values. (After ref. ).

Figure 19. Figure 19.

Integrated model for analysis of water–blood O2 transfer in fish gills. The exchange unit comprises the water–blood tissue barrier with one‐half of the interlamellar water flow and one‐half of the intralamellar blood flow. Axial extension (Y) is from water inflow and blood outflow at Y= 0 to water outflow and blood inflow at Y = 1. Water flow is with parabolic transversal flow profile (X direction), whereas blood is axially mixed. PO2 profiles are schematically shown. (After ref. ).

Figure 20. Figure 20.

Schematic explanation of alveolar–arterial differences (AaD) caused by unequal distribution of a to . Indicated are compartments I and II with their gas and blood partial pressures (below) as well as the P values in mixed gas and blood (m). AaD, visualized by open arrows, are qualitatively similar but quantitatively different for O2 and CO2. (A) Equal distribution, no AaD. (B) Unequal a/ distribution and AaD because of different flow‐weighing of gas and blood. (C) Shunt. Compartment II has no ventilation; its exiting blood is unchanged mixed venous blood. (D) Alveolar dead space; compartment II has no blood flow; its ventilation is alveolar dead space ventilation, adding unchanged inspired gas expired from compartment I. (After ref. ).

Figure 21. Figure 21.

Analysis of the effects of unequal distribution of a to upon alveolar gas exchange in the PO2‐PCO2 diagram. In (A) blood and gas R lines and various gas and blood PCO2 and PO2 values are shown. The end‐tidal point (E′) is slightly below the gas R line (see text). In (B) the alveolar–arterial PO2 and PCO2 differences and their splitting into their components, “shunt‐like” effect and “alveolar‐dead space‐like” effect, are shown, along with the effect of anatomical dead space. (After ref. ).

Figure 22. Figure 22.

Unequal distribution of alveolar ventilation ( a) to blood flow ( ). (A) Multicompartment model approaching continuous a/ distribution. (B) Three‐compartment model with potentially the same O2 and CO2 exchange efficiency as the multicompartment model. The perfusion of compartments with very low to zero a/ acts as shunt. The alveolar ventilation of compartments with very high to infinite a/ is functionally equivalent to alveolar dead space ventilation. (After ref. ).

Figure 23. Figure 23.

Inert gas elimination by lungs with a/ inhomogeneity as function of the partition coefficient λ (βbg). (A) Homogeneous lung model. The curve Pa = Pc′ corresponds to equation . The same curve is inscribed in B, C, and D as dotted line. (B) Lung model with a/ inhomogeneity, symbolized by two compartments with differing a/ ratios. (C) Lung model with shunt and (physiological) dead space ventilation. (D) Lung model combining models B and C. (After ref. ).

Figure 24. Figure 24.

(A) Example of a plot of retention (Pa/P ) as function of the blood‐gas partition coefficient (λ), measured in humans by the multiple inert gas infusion technique. (B) a/ inhomogeneity derived from the left example in terms of (continuous) distribution of blood flow to compartments with differing a/ ratios. (After ref. ).

Figure 25. Figure 25.

Gas transfer efficiency of lung models with D/ or D/( · βb) inhomogeneity. Lower row: PO2 profiles in capillary blood of the two compartments and PO2 in mixed arterial (end‐capillary) blood. (A) Homogeneous model. (B) Same total D as in (A) but unequally distributed to ; AaD is increased. (C) All D is allotted to the left compartment, blood flow to the right compartment acting as shunt flow. (After ref. ).

Figure 26. Figure 26.

(A) Schematic drawing of the eel swimbladder with pneumatic duct, secretory part of the swimbladder, and two retia mirabilia (after ref. ). (B) Schematic diagram of the vascular system of the swimbladder with rete mirabile and swimbladder epithelium. The symbols, at, ae, vi, ve denote arterial influx and efflux and venous influx and efflux of blood to the rete.

Figure 27. Figure 27.

Mechanisms that reduce the effective gas solubility in blood during passage through the swimbladder, leading to an increase in gas partial pressure. Lactic acid released from the gas gland cells leads to an increased inert gas partial pressure via the salting‐out effect (A) to an increased PO2via the Root effect (B) and to an increased PCO2via conversion of to CO2. Gas deposition, which would decrease gas concentration in the swimbladder vessels, is neglected.

Figure 28. Figure 28.

Schema of counter‐current enhancement of gas in the rete according to the classical concept. First panel: Schema of the counter‐current hairpin loop of the rete and gas gland. Black arrows designate flow direction and shaded arrows, solute movement from gas gland tissue into blood. Second panel: Solute concentration. Lower limb, arterial capillary; upper limb, venous capillary. Note that solute is assumed not to diffuse back in the rete. Third panel: Gas partial pressures increased (1) by addition of solute in the gland and (2) by back‐diffusion of gas from the venous (upper limb) to the arterial capillary. Fourth panel: Gas concentration is the same at corresponding positions in the arterial and venous capillaries, provided the system is closed in respect of fluid movement, which is assumed here. ai, ae, vi, and ve denote arterial influx and efflux and venous influx and efflux.

Figure 29. Figure 29.

Efficiency of the rete in enhancing inert gas partial pressure, calculated as the ratio of partial pressures in the arterial efflux and influx, Pae/Pai (see Fig. B). This efficiency is given by the conductance ratio D/( αa) (D, diffusing capacity of the rete; , blood perfusion; αa, physical solubility in rete afferent blood) and by the salting‐out effect, expressed as the solubility ratio, αva. The calculation assumes gas deposition to be zero. See text for further explanation.

Figure 30. Figure 30.

Present concept of metabolism of the gas gland cells and its influence on the physical solubility of inert gases or the release of gas from a chemical binding site in the blood. TCA, tricarboxylic acid cycle; PPS, pentose phosphate shunt. Open arrows indicate influence or possible influence on inert gas solubility and hemoglobin oxygen binding characteristics. Closed arrows indicate movement of substance.



Figure 1.

Illustration of the more important symbols used in this article. (A) Generalized symbols, used for modeling, fish gills, and bird lungs. , ventilation (air or water); , blood flow (perfusion); P1, Pe, Pv, Pa, partial pressures in inspired (i) and expired (e) media and in mixed venous (v) and arterialized (a) blood. (B) Mammalian symbols, used for mammalian lungs. e, total expired ventilation; d, dead space ventilation; a, alveolar ventilation; c, pulmonary capillary blood flow; sh, shunt blood flow; , total pulmonary blood flow; P, partial pressures in inspired gas (i), alveolar gas (a), end‐expired gas (e′), (mixed) expired gas (e); in mixed venous blood ( ) and arterial blood (a). (After ref. ).



Figure 2.

Partial pressure–concentration relationships of O2 and CO2 in air (left) and in seawater (containing bicarbonate/carbonate, right). CO2 in water refers to “total” CO2 (physically dissolved CO2, bicarbonate, and carbonate). The slope of the lines is the capacitance coefficient β.



Figure 3.

The CO2–O2 diagram for transport of respiratory gases by convection (of air or water) or diffusion (in air, water, or tissue), RQ being 0.9. The identity line (ΔPCO2: ΔPO2 = 1.0) is attained for convective transport in air at RQ = 1.0. Ranges for partial pressures of CO2 and O2 observed in arterialized blood of air breathers and water breathers are indicated by shaded areas. Dual (bimodal/trimodal) breathers are located in the intermediate range indicated by the double arrow. Note the different scales for PCO2 and PO2. (After ref. ).



Figure 4.

O2 dissociation curve and influencing parameters. In each graph, O2 content in blood (CO2) is on the ordinate, PO2 on the abscissa; a and v denote arterial and venous PO2. (A) O2 capacity is lower in blood with lower hemoglobin concentration. Dashed lines connect corresponding points of CO2 and PO2 in arterial and venous blood: slope is βb. (B) Cooperativity at the hemoglobin subunits results in higher βb compared with noncooperative binding (hyperbola—for example, in myoglobin). (C) Bohr effect results in effective dissociation curve that is steeper than that of the pH of either the arterial or the venous blood. (D) Moving the curve to the left or right, thereby changing P50 to P′50 or P″50, changes the slope βb between the given arterial PO2 and the venous PO2. (After ref. ).



Figure 5.

Schematic anatomy of the gill apparatus in teleost fish. (A) Gill arches covered by the operculum. (B) Section of a gill arch carrying filaments and secondary lamellae; direction of water flow shown by arrow. (C) Section of a filament with secondary lamellae; counter‐current flow of water and blood shown by arrows. (D) Cross section of two adjacent secondary lamellae and the interposed interlamellar water space. (After ref. ).



Figure 6.

Schematic anatomy of the respiratory apparatus in birds. (A) Lung and the air sacs. (B) Connections of the air sacs (AS) to the bronchial system; arrow indicates direction of air flow. (C) Section of the lung. (D) Section of periparabronchial tissue (para‐bronchial lumen on the left), showing the blood and air capillary networks. (After ref. ).



Figure 7.

Models for gas exchange organs in vertebrates and partial pressures in medium (water or air) and blood. Profiles in medium, between the entrance to (i) and the exit from (e) the organ, as well as in blood, between venous (v) and arterial (a) values, are indicated. (After ref. ).



Figure 8.

Partial pressures in medium (expired, Pe, or alveolar, Pa, respectively) and blood (arterialized or arterial, Pa) leaving the gas exchange area, relative to the medium (Pi and blood Pv) entering the gas exchange area, as functions of the ventilatory/perfusive conductance ratio, ( · βw)/( · βb), for three models (no diffusion limitation). In (B) and (C), the dotted line marks the curve for model (A) and the shaded area, the blood–gas overlap region, where the ratio (Pe – Pa)/(Pi – Pv) is negative. (After ref. ).



Figure 9.

Equivalence between the effects of conductance mismatch and shunt in the counter‐current system, assuming Pi = 100 and Pv = 60 units (no diffusion limitation). In (B), the ideal system with X = ( · βw)/( · βb) = 1. In (A, upper figure), mismatch is produced by doubling perfusive conductance, which leads to ( · βw)/( · βb) < 1 and lowers Pa to 80. The same effect is obtained when the extra blood flow is channeled through a blood shunt, whereby ideal matching conditions in the gas exchange compartment are restored (A, lower figure). In (C), a mismatch is created by doubling water flow conductance, whereby ( · βw)/( · βb) > 1 and Pc = 80. The same effect is produced by a water shunt. (After ref. ).



Figure 10.

Total conductance, Gtot, as function of diffusive conductance, D (A), and perfusive conductance, · βb (B). The limiting cases of pure perfusion and diffusion limitation are marked by broken lines. (After ref. ).



Figure 11.

Diffusion–perfusion limitation in alveolar–capillary transfer of various gases. Center: D/( · βb) ratio on logarithmic scale. Left: Perfusion and diffusion limitation areas are marked by different hatching; end of limitation area is taken at L = 0.05 (Table ). Right: Approximate location of inert and chemically bonded gases for alveolar–capillary transfer in normal human lungs in resting conditions. (After ref. ).



Figure 12.

Schematic representation of stratification. Density of stippling in lung models visualizes partial pressure (or concentration) of a gas (for example, CO2). The concentration profile of a gas with highest inspired value (for example, O2) is also shown. E′ denotes end‐expired gas. (After ref. ).



Figure 13.

Models to show the origin of alveolar‐arterial differnces for CO2 and O2 (AaD) in lungs with incomplete gas mixing in alveolar space. Gas‐blood diffusion is assumed to be nonlimiting. Density of stippling marks concentration of CO2. (A) Model with two compartments ventilated in series. AaD is due to the fact that end‐expired gas (A′) originates in the proximal compartment (1) only, whereas arterial blood is a mixture. (B) Like (A), but only the distal compartment (2) is perfused. An AaD arises because end‐expired gas (A′) is derived from the proximal compartment (1) and arterial blood from the distal compartment (2). (After ref. ).



Figure 14.

Simplified lung model for analysis of incomplete intra‐pulmonary gas mixing (stratification). In analogy to models (B) of Figs. and , the partial pressure difference (Pe′ – Pa) is due to finite Gmix and the difference Pa – Pa to finite D. (After ref. ).



Figure 15.

Partial pressure profiles of O2 in avian air capillary model. In spite of considerable fall of PO2 along the air capillary, arterial PO2 (Pa) is close to parabronchial PO2 (Ppb) because of the distal‐to‐proximal direction of capillary blood flow along the air capillary. The counter‐current‐like behavior is illustrated by the gas–blood PO2 overlap. (After ref. ).



Figure 16.

Fish gill model and characteristic measurements. (A) Model for a row of secondary lamellae on a gill filament. The spatial axes x, y, and z serve for orientation of the cross sections in the other quadrants. aff and eff are crosssectioned afferent and efferent arteries (both running in the x direction). (B) Cross section of the secondary lamellae parallel to the filament surface. (1) Length of the secondary lamella, (2b) width of the interlamellar water space. (C) Cross section of the secondary lamellae along the filament length. The secondary lamellae of adjacent filaments are shown by broken lines. (h) Height of the secondary lamella. (D) The trapezoidal lamella. (lo) Length of the base of the secondary lamella; γ, base‐to‐top tapering factor of the secondary lamella. (After ref. ).



Figure 17.

Water velocity and PO2 profiles in model for interlamellar space. PO, PO2 on plate surface; Pi, PO2 of inspired water; e, PO2 of mixed expired water. (A) Model showing parabolic velocity profiles (marked by hatching) for base, middle plane, and top. Three transverse sections (1, entry; 2, middle; 3, exit) are indicated. a and b refer to vertical sections in the y–z plane, in the middle and toward one side, respectively. (B) Longitudinal (y direction) PO2 profiles in planes a and b (at a fixed z value). (C) Vertical (z direction) PO2 profiles in planes 1, 2, and 3 (at a fixed x value). (D) Transverse (x direction) PO2 profiles in planes 1, 2, and 3 (at a fixed z value). (After ref. ).



Figure 18.

Inefficiency of O2 equilibration (ε) as a function of ϕ for selected values of tapering (γ). Stippled area: range of estimated γ values. (After ref. ).



Figure 19.

Integrated model for analysis of water–blood O2 transfer in fish gills. The exchange unit comprises the water–blood tissue barrier with one‐half of the interlamellar water flow and one‐half of the intralamellar blood flow. Axial extension (Y) is from water inflow and blood outflow at Y= 0 to water outflow and blood inflow at Y = 1. Water flow is with parabolic transversal flow profile (X direction), whereas blood is axially mixed. PO2 profiles are schematically shown. (After ref. ).



Figure 20.

Schematic explanation of alveolar–arterial differences (AaD) caused by unequal distribution of a to . Indicated are compartments I and II with their gas and blood partial pressures (below) as well as the P values in mixed gas and blood (m). AaD, visualized by open arrows, are qualitatively similar but quantitatively different for O2 and CO2. (A) Equal distribution, no AaD. (B) Unequal a/ distribution and AaD because of different flow‐weighing of gas and blood. (C) Shunt. Compartment II has no ventilation; its exiting blood is unchanged mixed venous blood. (D) Alveolar dead space; compartment II has no blood flow; its ventilation is alveolar dead space ventilation, adding unchanged inspired gas expired from compartment I. (After ref. ).



Figure 21.

Analysis of the effects of unequal distribution of a to upon alveolar gas exchange in the PO2‐PCO2 diagram. In (A) blood and gas R lines and various gas and blood PCO2 and PO2 values are shown. The end‐tidal point (E′) is slightly below the gas R line (see text). In (B) the alveolar–arterial PO2 and PCO2 differences and their splitting into their components, “shunt‐like” effect and “alveolar‐dead space‐like” effect, are shown, along with the effect of anatomical dead space. (After ref. ).



Figure 22.

Unequal distribution of alveolar ventilation ( a) to blood flow ( ). (A) Multicompartment model approaching continuous a/ distribution. (B) Three‐compartment model with potentially the same O2 and CO2 exchange efficiency as the multicompartment model. The perfusion of compartments with very low to zero a/ acts as shunt. The alveolar ventilation of compartments with very high to infinite a/ is functionally equivalent to alveolar dead space ventilation. (After ref. ).



Figure 23.

Inert gas elimination by lungs with a/ inhomogeneity as function of the partition coefficient λ (βbg). (A) Homogeneous lung model. The curve Pa = Pc′ corresponds to equation . The same curve is inscribed in B, C, and D as dotted line. (B) Lung model with a/ inhomogeneity, symbolized by two compartments with differing a/ ratios. (C) Lung model with shunt and (physiological) dead space ventilation. (D) Lung model combining models B and C. (After ref. ).



Figure 24.

(A) Example of a plot of retention (Pa/P ) as function of the blood‐gas partition coefficient (λ), measured in humans by the multiple inert gas infusion technique. (B) a/ inhomogeneity derived from the left example in terms of (continuous) distribution of blood flow to compartments with differing a/ ratios. (After ref. ).



Figure 25.

Gas transfer efficiency of lung models with D/ or D/( · βb) inhomogeneity. Lower row: PO2 profiles in capillary blood of the two compartments and PO2 in mixed arterial (end‐capillary) blood. (A) Homogeneous model. (B) Same total D as in (A) but unequally distributed to ; AaD is increased. (C) All D is allotted to the left compartment, blood flow to the right compartment acting as shunt flow. (After ref. ).



Figure 26.

(A) Schematic drawing of the eel swimbladder with pneumatic duct, secretory part of the swimbladder, and two retia mirabilia (after ref. ). (B) Schematic diagram of the vascular system of the swimbladder with rete mirabile and swimbladder epithelium. The symbols, at, ae, vi, ve denote arterial influx and efflux and venous influx and efflux of blood to the rete.



Figure 27.

Mechanisms that reduce the effective gas solubility in blood during passage through the swimbladder, leading to an increase in gas partial pressure. Lactic acid released from the gas gland cells leads to an increased inert gas partial pressure via the salting‐out effect (A) to an increased PO2via the Root effect (B) and to an increased PCO2via conversion of to CO2. Gas deposition, which would decrease gas concentration in the swimbladder vessels, is neglected.



Figure 28.

Schema of counter‐current enhancement of gas in the rete according to the classical concept. First panel: Schema of the counter‐current hairpin loop of the rete and gas gland. Black arrows designate flow direction and shaded arrows, solute movement from gas gland tissue into blood. Second panel: Solute concentration. Lower limb, arterial capillary; upper limb, venous capillary. Note that solute is assumed not to diffuse back in the rete. Third panel: Gas partial pressures increased (1) by addition of solute in the gland and (2) by back‐diffusion of gas from the venous (upper limb) to the arterial capillary. Fourth panel: Gas concentration is the same at corresponding positions in the arterial and venous capillaries, provided the system is closed in respect of fluid movement, which is assumed here. ai, ae, vi, and ve denote arterial influx and efflux and venous influx and efflux.



Figure 29.

Efficiency of the rete in enhancing inert gas partial pressure, calculated as the ratio of partial pressures in the arterial efflux and influx, Pae/Pai (see Fig. B). This efficiency is given by the conductance ratio D/( αa) (D, diffusing capacity of the rete; , blood perfusion; αa, physical solubility in rete afferent blood) and by the salting‐out effect, expressed as the solubility ratio, αva. The calculation assumes gas deposition to be zero. See text for further explanation.



Figure 30.

Present concept of metabolism of the gas gland cells and its influence on the physical solubility of inert gases or the release of gas from a chemical binding site in the blood. TCA, tricarboxylic acid cycle; PPS, pentose phosphate shunt. Open arrows indicate influence or possible influence on inert gas solubility and hemoglobin oxygen binding characteristics. Closed arrows indicate movement of substance.

References
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Peter Scheid, Johannes Piiper. Vertebrate Respiratory Gas Exchange. Compr Physiol 2011, Supplement 30: Handbook of Physiology, Comparative Physiology: 309-356. First published in print 1997. doi: 10.1002/cphy.cp130105