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Inert Gas Transport in Blood and Tissues

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Abstract

This article establishes the basic mathematical models and the principles and assumptions used for inert gas transfer within body tissues—first, for a single compartment model and then for a multicompartment model. From these, and other more complex mathematical models, the transport of inert gases between lungs, blood, and other tissues is derived and compared to known experimental studies in both animals and humans. Some aspects of airway and lung transfer are particularly important to the uptake and elimination of inert gases, and these aspects of gas transport in tissues are briefly described. The most frequently used inert gases are those that are administered in anesthesia, and the specific issues relating to the uptake, transport, and elimination of these gases and vapors are dealt with in some detail showing how their transfer depends on various physical and chemical attributes, particularly their solubilities in blood and different tissues. Absorption characteristics of inert gases from within gas cavities or tissue bubbles are described, and the effects other inhaled gas mixtures have on the composition of these gas cavities are discussed. Very brief consideration is given to the effects of hyper‐ and hypobaric conditions on inert gas transport. © 2011 American Physiological Society. Compr Physiol 1:569‐592, 2011.

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Figure 1. Figure 1.

Single element capillary‐tissue model.

Figure 2. Figure 2.

Exponential wash‐in of inert gas in a perfused single tissue element. The tissue (and venous) partial pressure rises from zero asymptotically to arterial partial pressure. The rate constant is reduced by increased tissue volume, increased tissue‐gas partition coefficient, and decreased blood flow.

Figure 3. Figure 3.

Pv(t) calculated using both the PDE model (solid line) and the ODE model (broken line) for the uptake of the anesthetic gas nitrous oxide where Pa(t) has a step change from 0 to 1 at time t = 0. Showing the more rapid response in the PDE model. From Whiteley et al. 82, with permission

Figure 4. Figure 4.

Schematic representation of body compartments. VRG, vessel‐rich group; MG, muscle group; FG, fat group; and VPG, vessel‐poor group.

Figure 5. Figure 5.

(A) Compartmental venous and tissue partial pressure versus time after imposition of a constant arterial partial pressure of 1.0. At 60 min, the arterial partial pressure is set to zero. Red lines, vessel‐rich group; green lines, muscle group; gray lines, vessel‐poor group; and orange lines, fat group. Solid lines represent the anesthetic vapor desflurane, dotted lines represent ether. (B) The mixed venous partial pressures for the same simulation.

Figure 6. Figure 6.

The simulated arterial Pco2 responses to step changes in ventilatory frequency. The ventilatory frequency was increased or decreased by a factor of 1.5 for each model at t = 0. Gray line, normal lung model; black line, embolism model; and dashed line, emphysema model. The open circles represent end‐tidal points. Main figure −10 to 50 s. Inset figure 0 to 500 s. From Yem et al. 85, with permission

Figure 7. Figure 7.

Axial distribution of gas transport during inspiration (black columns) and expiration (gray columns) for a tidal breath of cyclopropane (A), ether (B), and acetone (C). Each flux has been normalized by the total inspiratory soluble gas flux. As the blood solubility of gas increases from cyclopropane to acetone, the distribution shifts from a sharp concentrated peak in the alveolar region for cyclopropane to a wider distribution that spreads throughout the airways for acetone. From Anderson et al. 2, with permission

Figure 8. Figure 8.

The digitized emphysema MIGET distribution (gray, open circles, left ordinate) and the recovered three‐compartment distributions showing for each inert gas, with solubility increasing from left to right (SF6 to acetone) demonstrating an increasing effect of the solubility of the inert gas and that the high areas are affected more than the normal areas for both slow and fast compartments. Open triangles, mid compartment; open squares, fast high compartment; and open circles, slow high compartment. DS, dead space. From Yem et al. 85, with permission

Figure 9. Figure 9.

(A) Compartmental venous and tissue partial pressure versus time after imposition of a constant inspired partial pressure of 1.0. At 60 min, the inspired partial pressure is set to zero. Red lines, vessel‐rich group; green lines, muscle group; and orange lines, fat group. Solid lines represent the anesthetic vapor desflurane, dotted lines represent ether. (B) The mixed venous partial pressures for the same simulation.

Figure 10. Figure 10.

Washout of desflurane (green), N2O (blue), and isoflurane (purple) and a 30:70 MAC ratio mixture of isoflurane and N2O (pink dashed) from the VRG after 60 and 120 min of exposure at 1.0 MAC inspired throughout. Partial pressures are normalized, that is, expressed as a fraction of the value at t = 0.

Figure 11. Figure 11.

Sample data from two experimental runs in one volunteer showing the decline in end‐tidal sevoflurane and halothane concentrations during rebreathing from a 1‐liter bag. Filled symbols, sevoflurane; open symbols, halothane. Solid lines show monoexponential model fits (y = a et/τ) for each set of data points. Concentrations are expressed relative to the first end‐tidal value recorded during rebreathing.

Figure 12. Figure 12.

When ventilation to an area of lung ceases, lung collapses at a rate dependent on the inspired gas composition. Shown is the time to collapse found when breathing various mixtures of O2 and N2O was modeled. Results are given for when hypoxic pulmonary vasoconstriction (HPV) was, and was not, incorporated into the model. As Fio2 decreases from 1.0, time for collapse decreases to a minimum at Fio2 = 0.5. Further decreases in Fio2 result in increase in time to collapse. When HPV was incorporated into the model, time to collapse was approximately the same with Fio2 = 1.0 as with Fio2 = 0.3. When HPV was not incorporated, collapse took about the same time with Fio2 = 1.0 as with Fio2 = 0.25. Inclusion of HPV in the model resulted in prolongation of time to collapse with increasing effect as Fio2 decreased. Maximal prolongation was at Fio2 = 0.2 (lowest Fio2 considered) when time to collapse was 50% longer with than without HPV incorporation. From Joyce et al. 40, with permission

Figure 13. Figure 13.

The Kety‐Schmidt method of prolonged N2O wash‐in to the brain via inhalation. Closed circles show arterial sampling; open circles show cerebral venous sampling.

Figure 14. Figure 14.

Venous concentration‐time profile following rapid intra‐arterial injection of a bolus of tracer.

Figure 15. Figure 15.

Transit time probability function, h(t) (upper trace), cumulative probability, H(t) (middle trace), and 1 – cumulative probability, 1 – H(t) (lower trace).

Figure 16. Figure 16.

Diffusion paths from the capillary to tissue for rapid, complete diffusive equilibration (bold arrows, large compartment) and slower, incomplete diffusive equilibrium (faint arrows, dashed compartment).

Figure 17. Figure 17.

The tissue response (dashed line) to a sinusoidally varying arterial inert gas partial pressure (solid line).



Figure 1.

Single element capillary‐tissue model.



Figure 2.

Exponential wash‐in of inert gas in a perfused single tissue element. The tissue (and venous) partial pressure rises from zero asymptotically to arterial partial pressure. The rate constant is reduced by increased tissue volume, increased tissue‐gas partition coefficient, and decreased blood flow.



Figure 3.

Pv(t) calculated using both the PDE model (solid line) and the ODE model (broken line) for the uptake of the anesthetic gas nitrous oxide where Pa(t) has a step change from 0 to 1 at time t = 0. Showing the more rapid response in the PDE model. From Whiteley et al. 82, with permission



Figure 4.

Schematic representation of body compartments. VRG, vessel‐rich group; MG, muscle group; FG, fat group; and VPG, vessel‐poor group.



Figure 5.

(A) Compartmental venous and tissue partial pressure versus time after imposition of a constant arterial partial pressure of 1.0. At 60 min, the arterial partial pressure is set to zero. Red lines, vessel‐rich group; green lines, muscle group; gray lines, vessel‐poor group; and orange lines, fat group. Solid lines represent the anesthetic vapor desflurane, dotted lines represent ether. (B) The mixed venous partial pressures for the same simulation.



Figure 6.

The simulated arterial Pco2 responses to step changes in ventilatory frequency. The ventilatory frequency was increased or decreased by a factor of 1.5 for each model at t = 0. Gray line, normal lung model; black line, embolism model; and dashed line, emphysema model. The open circles represent end‐tidal points. Main figure −10 to 50 s. Inset figure 0 to 500 s. From Yem et al. 85, with permission



Figure 7.

Axial distribution of gas transport during inspiration (black columns) and expiration (gray columns) for a tidal breath of cyclopropane (A), ether (B), and acetone (C). Each flux has been normalized by the total inspiratory soluble gas flux. As the blood solubility of gas increases from cyclopropane to acetone, the distribution shifts from a sharp concentrated peak in the alveolar region for cyclopropane to a wider distribution that spreads throughout the airways for acetone. From Anderson et al. 2, with permission



Figure 8.

The digitized emphysema MIGET distribution (gray, open circles, left ordinate) and the recovered three‐compartment distributions showing for each inert gas, with solubility increasing from left to right (SF6 to acetone) demonstrating an increasing effect of the solubility of the inert gas and that the high areas are affected more than the normal areas for both slow and fast compartments. Open triangles, mid compartment; open squares, fast high compartment; and open circles, slow high compartment. DS, dead space. From Yem et al. 85, with permission



Figure 9.

(A) Compartmental venous and tissue partial pressure versus time after imposition of a constant inspired partial pressure of 1.0. At 60 min, the inspired partial pressure is set to zero. Red lines, vessel‐rich group; green lines, muscle group; and orange lines, fat group. Solid lines represent the anesthetic vapor desflurane, dotted lines represent ether. (B) The mixed venous partial pressures for the same simulation.



Figure 10.

Washout of desflurane (green), N2O (blue), and isoflurane (purple) and a 30:70 MAC ratio mixture of isoflurane and N2O (pink dashed) from the VRG after 60 and 120 min of exposure at 1.0 MAC inspired throughout. Partial pressures are normalized, that is, expressed as a fraction of the value at t = 0.



Figure 11.

Sample data from two experimental runs in one volunteer showing the decline in end‐tidal sevoflurane and halothane concentrations during rebreathing from a 1‐liter bag. Filled symbols, sevoflurane; open symbols, halothane. Solid lines show monoexponential model fits (y = a et/τ) for each set of data points. Concentrations are expressed relative to the first end‐tidal value recorded during rebreathing.



Figure 12.

When ventilation to an area of lung ceases, lung collapses at a rate dependent on the inspired gas composition. Shown is the time to collapse found when breathing various mixtures of O2 and N2O was modeled. Results are given for when hypoxic pulmonary vasoconstriction (HPV) was, and was not, incorporated into the model. As Fio2 decreases from 1.0, time for collapse decreases to a minimum at Fio2 = 0.5. Further decreases in Fio2 result in increase in time to collapse. When HPV was incorporated into the model, time to collapse was approximately the same with Fio2 = 1.0 as with Fio2 = 0.3. When HPV was not incorporated, collapse took about the same time with Fio2 = 1.0 as with Fio2 = 0.25. Inclusion of HPV in the model resulted in prolongation of time to collapse with increasing effect as Fio2 decreased. Maximal prolongation was at Fio2 = 0.2 (lowest Fio2 considered) when time to collapse was 50% longer with than without HPV incorporation. From Joyce et al. 40, with permission



Figure 13.

The Kety‐Schmidt method of prolonged N2O wash‐in to the brain via inhalation. Closed circles show arterial sampling; open circles show cerebral venous sampling.



Figure 14.

Venous concentration‐time profile following rapid intra‐arterial injection of a bolus of tracer.



Figure 15.

Transit time probability function, h(t) (upper trace), cumulative probability, H(t) (middle trace), and 1 – cumulative probability, 1 – H(t) (lower trace).



Figure 16.

Diffusion paths from the capillary to tissue for rapid, complete diffusive equilibration (bold arrows, large compartment) and slower, incomplete diffusive equilibrium (faint arrows, dashed compartment).



Figure 17.

The tissue response (dashed line) to a sinusoidally varying arterial inert gas partial pressure (solid line).

References
 1. Albert MS, Cates GD. Biological magnetic resonance imaging using laser‐polarized 129xe. Nature 370: 199‐201, 1994.
 2. Anderson JC, Babb AL, Hlastala MP. Modeling soluble gas exchange in the airways and alveoli. Ann Biomed Eng 31: 1402‐1422, 2003.
 3. Anderson JC, Hlastala MP. Breath tests and airway gas exchange. Pulm Pharmacol Ther 20: 112‐117, 2007.
 4. Anderson JC, Hlastala MP. Impact of airway gas exchange on the multiple inert gas elimination technique: Theory. Ann Biomed Eng 38: 1017‐1030, 2010.
 5. Armstrong HG. The origin of space medicine. U S Armed Forces Med J 10: 389‐392, 1959.
 6. Baker AB, Colliss JE, Cowie RW. Effect of varying inspiratory flow waveform and time in intermittent positive pressure ventilation II: Various physiological variables. Br J Anaesth 49: 1221‐1234, 1977.
 7. Baker AB, McGinn A, Joyce C. Effect on lung volumes of oxygen concentration when breathing is restricted. Br J Anaesth 70: 259‐266, 1993.
 8. Baker AB, Restall R. Changes in residual volume following oxygen breathing. Br J Anaesth 55: 817‐823, 1983.
 9. Baumgardner JE, Markstaller K, Pfeiffer B, Doebrich M, Otto CM. Effects of respiratory rate, plateau pressure and positive end‐expired pressure on PaO2 oscillations after saline lavage. Am J Respir Crit Care Med 166: 1556‐1562, 2002.
 10. Benavides R, Maze M, Franks NP. Expansion of gas bubbles by nitrous oxide and xenon. Anesthesiology 104: 299‐302, 2006.
 11. Bergman NA. Cyclic variations in blood oxygenation with the respiratory cycle. Anesthesiology 22: 900‐908, 1961.
 12. Bohr C. Ueber die Lungenathmung. Skand Arch Physiol 2: 236‐268, 1891.
 13. Burkard ME, Van Liew HD. Effects of physical properties of the breathing gas on decompression‐sickness bubbles. J Appl Physiol 79: 1828‐1836, 1995.
 14. Cekic O, Ohji M. Intraocular gas tamponades. Semin Ophthalmol 15: 3‐14, 2000.
 15. Chortkoff BS, Laster MJ, Koblin DD, Shahram TS, Eger EI, Halsey MJ. Pharmacokinetics do not explain the absence of an anesthetic effect of perfluoropropane or perfluoropentane. Anesth Analg 79 234‐237, 1994.
 16. Connor CW, Philip JH. The Severinghaus square root of time relationship for anesthetic uptake and its implications for the stability of compartmental pharmacokinetics. Physiol Meas 29: 685‐701, 2008.
 17. Cowles AL, Borgstedt HH, Gillies AJ. A simplified digital method for predicting anesthetic uptake and distribution. Comput Biol Med 3: 385‐395, 1973.
 18. Duhamel G, Choquet P, Grillon E, Lamalle L, Leviel J‐L, Ziegler A, Constantinesco A. Xenon‐129 MR imaging and spectroscopy of rat brain using arterial delivery of hyperpolarized xenon in a lipid emulsion. Magn Reson Med 46: 208‐202, 2001.
 19. Eger EI. A mathematical model of uptake and distribution. In: Papper EM, Kitz RJ, editors. Uptake and Distribution of Anesthetic Agents. New York: McGraw Hill, 1963, p. 72‐87.
 20. Eger EI, Saidman LJ. Illustrations of inhaled anesthetic uptake, including intertissue diffusion to and from fat. Anesth Analg 100: 1020‐1033, 2005.
 21. Eger EI, Shafer SL. Tutorial: Context‐sensitive decrement times for inhaled anesthetics. Anesth Analg 101: 688‐696, 2005.
 22. Enghoff H. Volumen inefficax, Bemerkungen zur Frage des schadlichen Raumes. Upsala Lakareforen Forh 44: 191‐218, 1938.
 23. Evans JW, Cantor DG, Norman JR. The dead space in a compartmental lung model. Bull Math Biophys 29: 711‐718, 1967.
 24. Evans JW, Wagner PD. Limits on VA/Q distributions from analysis of experimental inert gas elimination. J Appl Physiol 42: 889‐898, 1977.
 25. Feihl F, Eckert P, Brimioulle S, Jacobs O, Schaller MD, Melot C, Naeije R. Permissive hypercapnia impairs pulmonary gas exchange in the acute respiratory distress syndrome. Am J Respir Crit Care Med 162: 209‐215, 2000.
 26. Fiserova‐Bergerova V, Diaz ML. Determination and prediction of tissue‐gas partition coefficients. Int Arch Occup Environ Health 58: 75‐87, 1986.
 27. Folgering H, Smolders FDJ, Kreuzer F. Respiratory oscillations of arterial Po2 and their effects on the ventilatory controlling system in the cat. Pflugers Arch 375: 1‐7, 1978.
 28. Forster RE. Diffusion factors in gases and liquids. In: Papper EM, Kitz RJ, editors. Uptake and Distribution of Anesthetic Agents. New York: McGraw‐Hill, 1963, p. 20‐29.
 29. Fortune JB, Wagner PD. Effects of common dead space on inert gas exchange in mathematical models of the lung. J Appl Physiol 47: 896‐906, 1979.
 30. Gandofer A, Kampik A. Expansion of intraocular gas due to reduced atmospheric pressure. Case report and review of literature. Ophthalmologe 97: 367‐370, 2000.
 31. Gavaghan DJ, Hahn CEW. A mathematical evaluation of the alveolar amplitude response technique. Respir Physiol 102: 105‐120, 1995.
 32. Goto T, Suwa K, Uezono S, Ichinose F, Uchiyama M, Morita S. The blood‐gas partition coefficient of xenon may be lower than generally accepted. Br J Anaesth 80: 255‐256, 1998.
 33. Grocott HP, Sato Y, Homi HM, Smith BE. The influence of xenon, nitrous oxide and nitrogen on gas bubble expansion during cardiopulmonary bypass. Eur J Anaesthesiol 22: 353‐358, 2005.
 34. Guenard H, Manier G, Castaing Y, Varene N. Series dead space for inert gases in healthy subjects. Pflugers Arch 403: 384‐387, 1985.
 35. Hahn CEW. Oxygen respiratory gas analysis by sine‐wave measurement: A theoretical model. J Appl Physiol 81: 985‐997, 1996.
 36. Hahn CEW, Farmery AD. Gas exchange modelling: No more gills please. Br J Anaesth 91: 2‐15, 2003.
 37. Hlastala MP. The alcohol breath test—A review. J Appl Physiol 84: 401‐408, 1998.
 38. Hlastala MP, McKenna P, Middaugh M, Robertson HT. Role of diffusion‐dependent gas inhomogeneity in gas exchange in the dog. Bull Eur Physiopathol Respir 18: 373‐380, 1982.
 39. Ingvar DH, Lassen NA. The blood flow of the cerebral cortex determined by krypton‐85. Acta Physiol Scand 54: 325‐338, 1962.
 40. Joyce CJ, Baker AB, Kennedy RR. Gas uptake from an unventilated area of lung: Computer model of absorption atelectasis. J Appl Physiol 74: 1107‐1116, 1993.
 41. Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anesthesia: A mathematical model. J Appl Physiol 86: 1116‐1125, 1999.
 42. Kapitan K. Information content of the multibreath nitrogen washout: Effects of experimental error. J Appl Physiol 68: 1621‐1627, 1990.
 43. Kety SS. Measurement of regional circulation by the local clearance of radioactive sodium. Am Heart J 38: 321‐328, 1949.
 44. Kety SS. The physiological and physical factors governing the uptake of anesthetic gases by the body. Anesthesiology 11: 517‐526, 1950.
 45. Kety SS. The theory and applications of exchange of inert gas at the lungs and tissues. Pharmacol Rev 3: 1‐41, 1951.
 46. Kety SS, Schmidt CF. The nitrous oxide method for the quantitative determination of cerebral blood flow in man: Theory, procedure and normal values. J Clin Invest 27: 476‐484, 1948.
 47. Kjærgaard S, Rees SE, Nielsen JA, Freundlich M, Thorgaard P, and Andreassen S. Modelling of hypoxaemia after gynaecological laparotomy. Acta Anaesthesiol Scand 45: 349‐356 2001.
 48. Kumar KV, Waligora JM, Powell MR. Epidemiology of decompression sickness under simulated space extravehicular activities. Aviat Space Environ Med 64: 1032‐1039, 1993.
 49. Lewis SM, Evans JW, Jalowayski AA. Continuous distributions of specific ventilation recovered from inert gas washout. J Appl Physiol 44: 416‐423, 1978.
 50. Lindholm P, Lundgren CE. The physiology and pathophysiology of human breath‐hold diving. J Appl Physiol 106: 284‐292, 2009.
 51. MacFall JR, Charles HC, Black RD, Middleton H, Swartz JC, Saam B, Driehuys B, Erickson C, Happer W, Cates GD, Johnson GA, Ravin CE. Human lung air spaces: Potential for MR imaging with hyperpolarized He‐3. Radiology 200: 553‐558, 1996.
 52. Mapleson WW. An electric analogue for uptake and exchange of inert gases and other agents. J Appl Physiol 18: 197‐204, 1963.
 53. Mapleson WW. Circulation‐time models of the uptake of inhaled anaesthetics and data for quantifying them. Br J Anaesth 45: 319‐333, 1973.
 54. Meier P, Zierler KL. On the theory of the indicator‐dilution method for measurement of blood flow and volume. J Appl Physiol 6: 731‐744, 1954.
 55. Meyer M, Schuster K‐D, Schulz H, Mohr M, Piiper J. Alveolar slope and dead space of He and SF6 in dogs: Comparison of airway and venous loading. J Appl Physiol 69: 937‐944, 1990.
 56. Muth C‐M, Ehrmann U, Radermacher P. Physiological and clinical aspects of apnea diving. Clin Chest Med 26: 381‐394, 2005.
 57. Nye R. Theoretical limits to measurement of uneven ventilation. J Appl Physiol 16: 1115‐1123, 1961.
 58. Paterson S, Mackay D. Correlation of tissue, blood, and air partition coefficients of volatile organic chemicals. Br J Ind Med 46: 321‐328, 1989.
 59. Perl W, Rackow H, Salanitre S, Wolf GL, Epstein RM. Intertissue diffusion effect for inert fat‐soluble gases. J Appl Physiol 20: 621‐627, 1965.
 60. Philip JH. Gasman‐ Understanding Anesthesia Uptake and Distribution. Menlo Park, CA: Addison‐Wesley, 1984.
 61. Philip JH. Gasman‐ Computer Program. Chestnut Hill, MA: Med Man Simulations Inc., 2002.
 62. Purves MJ. Fluctuations of arterial oxygen tension which have the same period as respiration. Respir Physiol 1: 281‐296, 1966.
 63. Rackow H, Salanitre E, Epstein RM, Wolf GL, Perl W. Simultaneous uptake of N2O and cyclopropane in man as a test of compartment model. J Appl Physiol 20: 611‐620, 1965.
 64. Radermacher P, Falke KJ, Park YS, Ahn DW, Hong SK, Qvist J, Zapol WM. Nitrogen tensions in brachial vein blood of Korean ama divers. J Appl Physiol 73: 2592‐2595, 1992.
 65. Rees SE, Kjærgaard S, Andreassen S, Hedenstierna G. Reproduction of MIGET retention and excretion data using a simple mathematical model of gas exchange in lung damage caused by oleic acid infusion. J Appl Physiol 101: 826‐832, 2006.
 66. Rees SE, Kjærgaard S, Thorgaard P, Malczynski J, Toft E, Andreassen S. The Automatic Lung Parameter Estimator (ALPE) system: Non‐invasive estimation of pulmonary gas exchange parameters in 10–15 min. J Clin Monit Comput 17: 43‐52, 2002.
 67. Reinelt H, Schirmer U, Marx T, Topalidis P, Schmidt M. Diffusion of xenon and nitrous oxide into the bowel. Anesthesiology 94: 475‐477, 2001.
 68. Schilder DP, Roberts A, Fry DL. Effect of gas density and viscosity on the maximal expiratory flow‐volume relationship. J Clin Invest 42: 1705‐1713, 1963.
 69. Severinghaus JW. The rate of uptake of nitrous oxide in man. J Clin Invest 33: 1183‐1189, 1954.
 70. Shin HW, Condorelli P, Rose‐Gottron CM, Cooper DM, George SC. Probing the impact of axial diffusion on nitric oxide exchange dynamics with heliox. J Appl Physiol 97: 874‐882, 2004.
 71. Suwa K, Bendixen HH. A mathematical analysis of physiological dead space in a lung model. J Appl Physiol 24: 549‐555, 1968.
 72. Swanson SD, Rosen MS, Agronoff BW, Coulter KP, Welsh RC, Chupp TE. Brain MRI with laser‐polarized 129‐Xe. Mag Reson Med 38: 695‐698, 1997.
 73. Talbot NP, Farmery AD, Dorrington KL. End‐tidal sevoflurane and halothane concentrations during simulated airway occlusion in healthy humans. Anesthesiology 111: 287‐292, 2009.
 74. Tezlaff K, Thorsen E. Breathing at depth: Physiologic and clinical aspects of diving while breathing compressed gas. Clin Chest Med 26: 355‐380, 2005.
 75. Tokics L, Strandberg Å, Brismar B, Lundquist H, Hedenstierna G. Computerized tomography of the chest and gas exchange measurements during ketamine anaesthesia. Acta Anaesthesiol Scand 31: 684‐692, 1987.
 76. Wagner PD. Peripheral inert‐gas exchange. In: Geiger SR, editor. Handbook of Physiology: The Respiratory System. Baltimore, MD: Williams & Wilkins, 1985‐1987, p. 257‐281.
 77. Wagner PD, Laravuso RB, Uhl RR, West JB. Continuous distribution of ventilation‐perfusion ratios in normal subjects breathing air and 100% O2. J Clin Invest 54: 54‐68, 1974.
 78. Wagner PD, Naumann PF, Laravuso RB. Simultaneous measurement of eight foreign gases in blood by gas chromatography. J Appl Physiol 36: 600‐605, 1974.
 79. Wagner PD, Saltzman HA, West JB. Measurement of continuous distributions of ventilation‐perfusion ratios: Theory. J Appl Physiol 36: 588‐599, 1974.
 80. West JB, Wagner PD. Pulmonary gas exchange. In: West JB, editor. Bioengineering Aspects of the Lung. New York: Marcel Dekker, 1977, p. 361‐454.
 81. Whiteley JP, Farmery AD, Gavaghan DJ, Hahn CEW. A tidal ventilation model for oxygenation in respiratory failure. Respir Physiol Neurobiol 136: 77‐88, 2003.
 82. Whiteley JP, Gavaghan DJ, Hahn CEW. Modelling inert gas exchange in tissue and mixed‐venous blood return to the lungs. J Theor Biol 209: 431‐443, 2001.
 83. Whiteley JP, Turner MJ, Baker AB, Gavaghan DJ, Hahn CEW. The effects of ventilation pattern on carbon dioxide transfer in three computer models of the airways. Respir Physiol Neurobiol 131: 269‐284, 2002.
 84. Williams EM, Hamilton R, Sutton L, Hahn CEW. Measurement of respiratory parameters by using inspired oxygen sinusoidal forcing signals. J Appl Physiol 81: 998‐1006, 1996.
 85. Yem SJ, Turner MJ, Baker AB, Young IH, Crawford ABH. A tidally breathing model of ventilation, perfusion and volume in normal and diseased lungs. Br J Anaesth 97: 718‐731, 2006.
 86. Zhou X, Mazzanti ML, Chen JJ, Tzeng YS, Mansour JK, Gereige JD, Venkatesh AK, Sun Y, Mulkern RV, Albert MS. Reinvestigating hyperpolarized 129‐Xe longitudinal relaxation time in the rat brain with noise considerations. NMR Biomed 21: 217‐225, 2008.
 87. Zierler KL. Equations for measuring blood flow by external monitoring of radioisotopes. Cir Res 16: 309‐321, 1965.
 88. Zuntz N. Zur Pathogenese und Therapie der durch rasche Luftdrukaenderungen erzeugten Krankheiten. Fortschr Med 15: 632‐639, 1897.
 89. Zwart A, Smith NT, Beneken JEW. Multiple models approach to uptake and distribution of halothane. Comput Biomed Res 5: 228‐238, 1972.
 90. Zwart A, van Dieren A. Monitoring and control aspects during halothane anesthesia: Some results of combined model simulation and animal experiments. In: Progress Report. Utrecht, Germany: Institute of Medical Physics TNO, 1974.
 91. Zwart A, van Dieren A. A simple and non‐invasive method to determine the ventilation‐perfusion ratio of the lung and the effective lung perfusion. Acta Anaesthet Belg 26: 53‐64, 1975.

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A. Barry Baker, Andrew D. Farmery. Inert Gas Transport in Blood and Tissues. Compr Physiol 2011, 1: 569-592. doi: 10.1002/cphy.c100011