The flow diverting effectiveness ofHPV may depend not only on some of the factors indicated above, but also on the cause of the poor ventilation. For example, in pneumonia, both the host and pathogen mediated inflammatory response would be expected to affect local HPV and/or its modulation (6, 41, 91). In addition, the extent to which the arteries serving the region are mechanically influenced by the alteration in local lung mechanics responsible for the local hypoventilation may have an effect as a consequence ofway the vessels are imbedded within the lung parenchyma. Pulmonary vessels have been categorized as alveolar and extra-alveolar vessels. The designation is based on how they are affected by lung inflation. Due to interdependence between the vessel walls and surrounding parenchyma, lung inflation distends extra-alveolar vessels, which include the larger intrapulmonary arteries. Thus, an increase in lung volume would oppose extra-alveolar vessel HPV (15). The alveolar vessels include the capillaries within the alveolar septa that stretch and narrow as the alveolar wall circumference increases with inflation. Thus, an increase in volume would augment alveolar vessel HPV. The small hypoxia responsive arteries are located close to or within the transition region between the larger extra-alveolar arteries and the smaller alveolar capillaries. The extent to which these vessels behave more like extra-alveolar or alveolar vessels may determine the extent to which local distortions ofthe lung parenchyma will augment or oppose the HPV (15), and there are species variations, with hypoxia responsive vessels being mainly extra-alveolar in the dog (15), rat (7), and ferret (15, 86), but more alveolar in the sheep and pig (15, 86). In the rat at least, the growth of vascular smooth muscle into smaller vessels, that occurs during chronic hypoxia (50), is accompanied by a transition in the behavior of the hypoxic response from that indicative of an extra-alveolar site of action to that of an alveolar site of action (7). In addition, in any region in which the alveoli are disconnected from the flow of tracheal air, such as in a region of atelectasis or behind an obstructed airway, the vessels within the region are subject to the forces transmitted through the surrounding parenchyma in a manner similar to the interdependence affecting the extra-alveolar vessels. Thus, the extent to which the hypoxia responsive vessels are subjected to these forces will impact on the extent to which HPV is effective in reducing regional flow (15).
Between-species heterogeneities (72) in the intensity of HPV are difficult to evaluate at least in part because the modulation of the hypoxic response may vary among species depending on the preparation used in the study. For example in isolated lung experiments the dog came out as a poorly responding species (72), whereas in situ dog lungs responded well to hypoxia (62, 63), much like isolated dog lungs treated with cyclooxygenase inhibitors (3, 15). One between species heterogeneity that has a teleological rationale is the correlation between the effectiveness of the response and the extent of collateral ventilation, which holds for several species studied (33). The rationale is that the presence of collateral ventilation, which would tend to diminish the impact of small airway obstruction on local ventilation, would also decrease the importance of HPV as a means of controlling V/Q mismatch.
It may be surprising that, given the importance of HPV in the fetus, the intensity of HPV typically increases with post-natal age (24, 76). This may be at least partly because the transition from fetal to neonatal circulation, in which increased pulmonary blood flow is a key element, involves mechanisms that attenuate HPV (1, 28, 38, 51). Postnatal development also involves extension of smooth muscle into smaller arteries (67), in keeping with a transition of the hypoxic response from that providing the tone required to keep the flow to the lungs low during the globally and normally low lung oxygen levels before birth to that providing local control of blood flow in the air breathing lung. HPV has been found to be both more (22) and less intense (65) than normal in lungs from mature animals chronically exposed to hypoxia, and the functional implications are not entirely obvious either way.
These and other heterogeneities certainly add complexity to the problem of understanding the physiological and pathophysiological implications ofHPV. In so doing they help to make the pursuit of that understanding challenging and exciting, as reflected in the many ingenious approaches that have been applied to the problem, only a very few of which could be represented in the available space.
Work from our laboratory presented in this chapter was supported by the NIH (HL-19298), the Department of Veterans' Affairs and the W. M. Keck Foundation.
1. Abman SH, Chatfield BA, Hall SL, and McMurtry IF. Role of endothelium-derived relaxing factor during transition of pulmonary circulation at birth. Am. J. Physiol. 1990; 259: H1921-
2. Altemeier WA, Robertson HT, and Glenny RW. Pulmonary gas-exchange analysis by using simultaneous deposition ofaerosolized and injected microspheres. J. Appl. Physiol. 1998; 85: 2344-2351.
3. Al-Tinawi A, Krenz GS, Rickaby DA, Linehan JH, and Dawson CA. Influence of hypoxia and serotonin on small pulmonary vessels. J. Appl. Physiol. 1994; 76: 56-64.
4. Anand IS, Prasad BAK, Chugh SS, Rao KRM, Cornfield DN, Milla CE, Singh N, Singh S, and Selvamurthy W. Effects of inhaled nitric oxide and oxygen in high-altitude pulmonary edema. Circulation 1998; 98: 2441-2445.
5. Archer AL, Huang JMC, Reeve HL, Hampl V, Tolarova S, Michelakis E, and Weir EK. Differential distribution ofelectrophysiologically distinct myocytes in conduit and resistance arteries determines their response to nitric oxide and hypoxia. Circ. Res. 1996; 78: 431-442.
6. Baboolal HA, Ichinose F, Ullrich R, Kawai N, Bloch KD, and Zapol WM. Reactive oxygen species scavengers attenuate endotoxin-induced impairment of hypoxic pulmonary vasconstriction in mice. Anesthesiology 2002; 97: 1227-1233.
7. Barer GR, Emery CJ, Bee D, and Wach RA. "Mechanisms of pulmonary hypertension: an overview." In The Pulmonary Circulation in Health and Disease, Will JA, Dawson CA, Weir EK, and Buckner CK, eds. Orlando, FL: Academic Press, Inc., 1987, pp. 409-422.
8. Barer G, Emery C, Stewart A, Bee D, and Howard P. Endothelial control of the pulmonary circulation in normal and chronically hypoxic rats. J. Physiol. 1993; 463: 1-16.
9. Berkov S. Hypoxic pulmonary vasoconstriction in the rat, the necessary role of angiotensin II. Circ. Res. 1974; 35:256-261.
10. Block ER, Herrera H, and Couch M. Hypoxia inhibits L-arginine uptake by pulmonary artery endothelial cells. Am. J. Physiol. 1995; 269: L574-L580.
11. Busch T, Bartsch P, Pappert D, Grunig E, Hildebrandt W, Elser H, Falke KJ, and Swenson ER. Hypoxia decreases exhaled nitric oxide in mountaineers susceptible to high-altitude pulmonary edema. Am. J. Respir. Crit. Care Med. 2001; 163: 368-373.
12. Chammas JH, Rickaby DA, Guarin M, Linehan JH, Hanger CC, and Dawson CA. Flow-induced vasodilation in the ferret lung. J. Appl. Physiol. 1997; 83:495-502.
13. Chirpaz-Oddou MF, Favre-Juvin A, Flore P, Eterradossi J, Delaire M, Grimbert F, and Therminarias A. Nitric oxide response in exhaled air during an incremental exhaustive exercise. J. Appl. Physiol. 1997; 82: 1311-1318.
14. Clough AV, Haworth ST, Ma W, and Dawson CA. Effects of hypoxia on pulmonary microvascular volume. Am. J. Physiol. Heart Circ. Physiol. 2000; 279: H1274-H1282.
15. Dawson CA. Role of pulmonary vasomotion in the physiology of the lung. Physiol. Rev. 1984, 64: 544-616.
16. Dawson CD, Krenz GS, and Linehan JH. "Complexity and Structure-Function relationships in the pulmonary arterial tree, Chapter 13." In Lung Biology in Health and Disease. Complexity in Structure and Function of the Lung, Hlastala MP and Robertson HT, eds. New York, NY: Marcel Dekker, Inc., 1998, pp. 401-427.
17. Droma Y, Hanaoka M, Ota M, Katsuyama Y, Koizumi T, Fujimoto K, Kobayashi T, and Kubo K. Positive association of the endothelial nitric oxide synthase gene polymorphisms with high-altitude pulmonary edema. Circulation 2002; 106: 826-830.
18. Droma Y, Ri-Li G, Tanaka M, Koizumi T, Hanaoka M, Miyahara T, Yamaguchi S, Okada K, Yoshikawa S, Fujimoto K, Matsuzawa Y, Kubo K, Kobayashi T, and Sekiguchi M. Acute hypoxic pulmonary vascular response does not accompany plasma endothelin-1 elevation in subjects susceptible to high altitude pulmonary edema. Intern. Med. 1996; 35: 257-260.
19. Duke HN. The site of action of anoxia on the pulmonary blood vessels of the cat. J. Physiol. 1954; 125: 373-382.
20. Duplain H, Sartori C, Leipri M, Egli M, Allemann Y, Nicod P, and Scherrer U. Exhaled nitric oxide in high-altitude pulmonary edema. Role in the regulation of pulmonary vascular tone and evidence for a role against inflammation. Am. J. Respir. Crit. Care Med. 2000; 162: 221-224.
21. Duplain H, Vollenweider L, Delabays A, Nicod P, Bartsch P, Sherrer U. Augmented sympathetic activation during short-term hypoxia and high altitude exposure in subjects susceptible to high -altitude pulmonary edema. Circulation 1999; 99: 1713-1718.
22. Eldridge MW, Podolsky A, Richardson RS, Johnson DH, Knight DR, Johnson EC, Hopkins SR, Michimata H, Grassi B, Feiner J, Kurdak SS, Bickler PE, Wagner PD, and Severinghaus JW. Pulmonary hemodynamic response to exercise in subjects with prior high-altitude pulmonary edema. J. Appl. Physiol. 1996; 81: 911-921.
23. Emery CJ, Bee, D, and Barer GR. Mechanical properties and reactivity of vessels in isolated perfused lungs of chronically hypoxic rats. Clin. Sci. 1981; 61: 569-583.
24. Fike CD and Hansen TN. Hypoxic vasoconstriction increases with postnatal age in lungs from newborn rabbits. Circ. Res. 1987; 60: 297-303.
25. Fishman AP. Hypoxia on the pulmonary circulation: how and where it acts. Circ. Res. 1976; 38: 221-231.
26. Glenny RW, Bernard S, Robertson HT, and Hlastala MP. Gravity is an important but secondary determinant of regional pulmonary blood flow in upright primates. J. Appl. Physiol. 1999; 86: 623-632.
27. Glenny RW, Robertson HT, and Hlastala MP. Vasomotor tone does not affect perfusion heterogeneity of gas exchange in normal primate lungs during normoxia. J. Appl. Physiol. 2000; 89: 2263-2267.
28. Gordon JB, Tod ML, Wetzel RC, McGeady ML, Adkinson NF Jr, and Sylvester JT. Age-dependent effects of indomethacin on hypoxic vasoconstriction in neonatal lamb lungs. Pediatr. Res. 1988; 23: 580-584.
29. Grant BJB. Effect of local pulmonary blood flow control on gas exchange theory. J. Appl. Physiol. 1982; 53: 1100-1109.
30. Hackett PH, Roach RC, Hartig GS, Green ER, and Levine BD. The effect of vasodilators on pulmonary hemodynamics in high altitude pulmonary edema: a comparison. Int. J. Sports Med. 1992; 13: S68-71.
31. Hakim TS. Flow-induced release of EDRF in the pulmonary vasculature: site ofrelease and action. Am. J. Physiol. 1994; 267: H363-369.
32. Hakim TS and Malik AB. Hypoxic vasoconstriction in blood and plasma perfused lungs. Respir. Physiol. 1988; 72: 109-121.
33. Hanson WL, Boggs DF, Kay JM, Hofmeister SE, and Wagner WW Jr. Collateral ventilation and pulmonary arterial smooth muscle in the coati. J. Appl. Physiol. 1993; 74: 2219-2224.
34. He L, Chang SW, de Montellano PO, Burke TJ, and Voelkel NF. Lung injury in Fischer but not Sprague-Dawley rats after short-term hyperoxia Am. J. Physiol. 1990; 259: L451-L458.
35. Helgesen KG and Bjertnaes L. The effect ofketanserin on hypoxia-induced vasoconstriction in isolated lungs. Int J Microcirc Clin Exp 1986; 5: 65-72.
36. Henderson KK, Wagner H, Favret F, Britton SL, Koch LG, Wagner PD, and Gonzalez NC. Determinants of maximal 02 uptake in rats selectively bred for endurance running capacity. J. Appl. Physiol. 2002; 93: 1265-1274.
37. Hillier SC, Graham JA, Hanger CC, Godbey PS, Glenny RW, and Wagner WW. Hypoxic vasoconstriction in pulmonary arterioles and venules. J. Appl. Physiol. 1997; 82:1084-1090.
38. Hislop AA, Springall DR, Buttery LDK, Pollock JS, and Haworth SG. Abundance of endothelial nitric oxide synthase in newborn intrapulmonary arteries. Arch. Dis. Child Fetal Neonatal 1995; 73: 17-21.
39. Hultgren HN. High altitude pulmonary edema: hemodynamic aspects. Int. J. Sports Med. 1997; 18: 20-25.
40. Hyman AL, Higashida RT, Spannhake EW, and Kadowitz PJ. Pulmonary vasoconstrictor responses to graded decreases in precapillary blood P02 in intact-chest cat. J. Appl. Physiol. 1981; 51: 1009-1016.
41. Ichinose F, Zapol WM, Sapirstein A, Ullrich R, Tager AM, Coggins K, Jones R, and Bloch KD. Attenuation of hypoxic pulmonary vasoconstriction by endotoxemia requires 5-lipoxygenase in mice. Circ. Res. 2001; 88: 832-838.
42. Ide H, Nakano H, Ogasa T, Osanal S, Kikuchi K, and Iwamoto J. Regulation of pulmonary circulation by alveolar oxygen tension via airway nitric oxide. J. Appl. Physiol. 1999; 87: 1629-1636.
43. Jensen KS, Micco AJ, Czartolomna J, Latham L, and Voelkel NF. Rapid onset of hypoxic vasoconstriction in isolated lungs. J. Appl. Physiol. 1992; 72: 2018-2023.
44. Johnson LR, Rush JWE, Turk,JR, Price EM, and Laughlin MH. Short-term exercise training increases ACh-induced relaxation and eNOS protein in porcine pulmonary arteries. J. Appl. Physiol. 2001; 90: 1102-1110.
45. Johnson W, Nohria A, Garrett L, Fang JC, and Igo J. Contribution of endothelin to pulmonary vascular tone under normoxic and hypoxic conditions. Am. J. Physiol. Heart Circ. Physiol. 2002; 283: H568-H575.
46. Juranek I, Suzuki H, Yamamoto S. Affinities of various mammalian arachidonate lipoxygenases and cyclooxygenases for molecular oxygen as substrate. Biochim. Biophys. Acta 1999; 1436: 509-518.
47. Kane DW, Tesauro T, Koizumi T, Gupta R, and Newman JH. Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors. J. Clin. Invest. 1994; 93: 677-683.
48. Kapanci Y, Costabella PM, Cerutti P, and Assimacopoulos A. Distribution and function of cytoskeletal proteins in lung cells with particular reference to "Contractile interstitial cells. Methods Achiev. Exp. Pathol. 1979; 9:1 47-168.
49. Kawashima A, Kubo K, Kobayashi T, and Sekiguchi M. Hemodynamic responses to acute hypoxia, hypobaria and exercise in subjects susceptible to high-altitude pulmonary edema. J. Appl. Physiol. 1989; 67: 1982-1989.
50. Kay JM. "Pulmonary vasculature and experimental pulmonary hypertension in animals." In The Pulmonary Circulation in Health and Disease, Will JA, Dawson CA, Weir EK, and Buckner CK, eds. Orlando, FL: Academic Press, Inc, 1987, pp. 41-56.
51. Konduri GG and Mattei J. Role of oxidative phosphorylation and ATP release in mediating birth-related pulmonary vasodilation in fetal lambs. Am. J. Physiol. Heart Circ. Physiol. 2002; 283: H1600-H1608.
52. Krenz GS and Dawson CA. Flow and pressure distributions in vascular networks consisting of distensible vessels. Am. J. Physiol. Heart Circ. Physiol. 2003; 284: H2192-H2203.
53. Landolt CC, Matthay MA, Albertine KH, Roos PJ, Wiener-Kronish JP, and Staub NC. Overperfusion, hypoxia, and increased pressure cause only hydrostatic pulmonary edema in anesthetized sheep. Circ. Res. 1983; 52: 335-341.
54. LeCrass TD and McMurtry IF. Nitric oxide production in the hypoxic lung. Am. J. Physiol. Lung Cell Mol. Physiol. 2001; 280: L575-L582.
55. Leeman M, DeBeyl VZ, Delcroix M, and Naeije R. Effects of endogenous nitric oxide on pulmonary vascular tone in intact dogs. Am. J. Physiol. 1994; 266: H2343-H2347.
56. Lejeune P, Vachiery JL, Leeman M, Brimioulle S, Hallemans R, Melot C, and Naeije R. Absence ofparasympathetic control ofpulmonary vascular pressure-flow plots in hyperoxic and hypoxic dogs. Respir. Physiol. 1989; 78: 123-133.
57. Liu Q, Sham SK, Shimoda LA, and Sylvester JT. Hypoxic constriction of porcine distal pulmonary arteries: endothelium and endothelin dependence. Am. J. Physiol. Lung Cell. Mol. Physiol. 2001; 280: L856-L865.
58. Lodato RF, Micael JR, and Murray PA. Absence of neural modulation of hypoxic pulmonary vasoconstriction in conscious dogs. J. Appl. Physiol. 1988; 65: 1481-1487.
59. Madden J, Dawson CA, and Harder DA. Hypoxia-induced activation in small isolated pulmonary arteries from the cat. J. Appl. Physiol. 1985; 59: 113-118.
60. Madden MC, Vender RL, and Friedman M. Effect of hypoxia on prostaglandin production in cultured pulmonary artery endothelium. Prostaglandins 1986; 31: 1049-1062.
61. Maggiorini M, Melot C, Pierre S, Pfeiffer F, Greve I, Sartori C, Lepori M, Hauser M, Scherrer U, and Naeije R. High-altitude pulmonary edema is initially caused by an increase in capillary pressure. Circulation 2001; 103: 2078-2083.
62. Mann CM, Domino KB, Walther SM, Glenny RW, Polissar NL, and Hlastala MP. Redistribution ofpulmonary blood flow during unilateral hypoxia in prone and supine dogs. J. Appl. Physiol. 1998; 84: 2010-2019.
63. Marshall BE, Marshall C, BenumofJ, and Saidman LJ. Hypoxic pulmonary vasoconstriction in dogs: effects of lung segment size and oxygen tension. J. Appl. Physiol. 1981; 51: 15431551.
65. McMurtry IF, Petrun MD, and Reeves JT. Lungs from chronically hypoxic rats have decreased pressor response to acute hypoxia. Am. J. Physiol. 1978; 235: H104-H109.
66. Melot C, Naeije R, Hallemans R, Lejeune P, and Mols P. Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man. Resp. Physiol. 1987; 68: 1127.
67. Michel RP, Gordon JB, and Chu K. Development of the pulmonary vasculature in newborn lambs: structure-function relationships. J. Appl. Physiol. 1991; 70: 1255-1264.
68. Nelin LD and Dawson CA. The effect of Nffl-nitro-L-arginine methylester on hypoxic vasoconstriction in the neonatal pig lung. Pediatr. Res. 1993; 34: 349-353.
69. Nelin LD, Thomas CJ, and Dawson CA. Effect of hypoxia on nitric oxide production in neonatal pigs. Am. J. Physiol. 1996; 271: H8-H14.
70. North AJ, Brannon TS, Wells LB, Campbell WB, and Shaul PW. Hypoxia stimulates prostacyclin synthesis in newborn pulmonary artery endothelium by increasing cyclooxygenase-1 protein. Circ. Res. 1994; 75: 33-40.
71. Ogasa T, Nakano H, Ide H, Yamamoto Y, Sasaki N, Osanai S, Akiba Y, Kikuchi K, and Iwamoto J. Flow-mediated release of nitric oxide in isolated perfused rabbit lungs. J. Appl. Physiol. 2001; 91: 363-370.
72. Peake MD, Harabin AL, Brennan NJ, and Sylvester JT. Steady-state vascular responses to graded hypoxia in isolated lungs of five species. J. Appl. Physiol. 1981; 51: 1214-1219.
73. Phillips CR, Giraud GD, and Holden WE. Exhaled nitric oxide during exercise: site of release and modulation by ventilation and blood flow. J. Appl. Physiol. 1996; 80: 1865-1871.
74. Pison U, Lopez FA, Heidelmeyer CF, Rossaint R, and Falke KJ. Inhaled nitric oxide reverses hypoxic pulmonary vasoconstriction without impairing gas exchange. J. App. Physiol. 1993; 74: 1287-1292.
75. Reid LM. The pulmonary circulation: remodeling in growth and disease. Am. Rev. Respir. Dis. 1979; 119: 531-546.
76. Rendas A, Branthwaite M, Lennod S, Reid L. Response of the pulmonary circulation to acute hypoxia in the growing pig. J. Appl. Physiol. 1982; 52: 811-814.
77. Rengasamy A and Johns RA. Determination of Km for oxygen of nitric oxide synthase isoforms. J. Pharmacol. Exp. Ther. 1996; 276: 30-33.
78. Salameh G, Karamsetty MR, Warburton RR, Klinger JR, Ou LC, and Hill NS. Differences in acute hypoxic pulmonary vasoresponsiveness between rat strains: role of endothelium. J. Appl. Physiol. 1999; 87: 356-362.
79. Sartori C, Vollenweider L, Loffler BM, Delabays A, Nicod P, Bartsch P, and Scherrer U. Exaggerated endothelin release in high-altitude pulmonary edema. Circulation 1999; 99: 2665-2668.
80. Schacterle RS, Adams JM, and Ribando RJ. A theoretical model of gas transport between arterioles and tissue. Microvasc. Res. 1991; 41: 210-228.
81. Scherrer U, Vollenweider L, Delabays A, Savcic M, Eichenberger U, Kleger G-R, Fikrle A, Ballmer PE, Nicod P, and Bartsch P. Inhaled nitric oxide for high-altitude pulmonary edema. N. Engl. J. Med. 1996; 334: 624-630.
82. Secomb TW and Pries AR. Information transfer in microvascular networks. Microcirculation 2002; 9: 377-387.
84. Shirai M, Shindo T, and Ninomiya I. ß-adrenergic mechanisms attenuate hypoxic pulmonary vasoconstriction during systemic hypoxia in cats. Am. J. Physiol. 1994; 266: H1777-H1785.
85. Sprague RS, Ellsworth ML, Stephenson AH, and Lonigro AJ. ATP: the red blood cell link to NO and local control of the pulmonary circulation. Am. J. Physiol. 1996; 271: H2717-H2722.
86. Sylvester, JT, Brower, RG, and Permutt, S. "Effects of hypoxic vasoconstriction on the mechanical interaction between pulmonary vessels and airways." In The Pulmonary Circulation in Health and Disease, Will JA, Dawson CA, Weir EK, and Buckner CK, eds. New York, NY: Academic Press, 1987, pp. 321-334.
87. Torre-Buenoi JR, Wagner PD, Saltzman HA, Gale GE, and Moon RE. Diffusion limitation in normal humans during exercise at sea level and simulated altitude. J. Appl. Physiol. 1985; 58: 989-995.
88. Vadula MS, Kleinman JG, and Madden JA. Effect of hypoxia and norepinephrine on cytoplasmic free Ca2+ in pulmonary and cerebral arterial myocytes. Am. J. Physiol. 1993; 265: L591-L597.
89. Van Grondelle A, Worthen GS, Ellis D, Mathias MM, Murphy RC, Strife RJ, Reeves JT, and VoelkelNF. Altering hydrodynamic variables influences PGI2 production by isolated lungs and endothelial cells. J. Appl. Physiol. 1984; 57: 388-395.
90. Von Euler US and Liljestrand G. Observations on the pulmonary arterial blood pressure in the cat. Acta Physiol. Scand. 1946; 12: 301-320.
91. Yaghi A, Paterson NAM, and McCormack G. Nitric oxide does not mediate the attenuated pulmonary vascular reactivity of chronic pneumonia. Am. J. Physiol. 1993; 265: H943-H948.
92. Yamaguchi K, Suzuki K, Naoki K, Nishio K, Sato N, Takeshita K, Kudo H, Aoki T, Suzuki Y, Miyata A, and Tsumura H. Response of intra-acinar pulmonary microvessels to hypoxia, hypercapnic acidosis, and isocapnic acidosis. Circ. Res. 1998; 82: 722-728.
93. Zhu D, Birks EK, Dawson CA, Patel M, Falck JR, Presberg K, Roman, RJ, and Jacobs, ER. Hypoxic pulmonary vasoconstriction is modified by P-450 metabolites. Am. J. Physiol. Heart Circ. Physiol. 2000; 279: H1526-H1533.
The editor notes with sadness the passing of Dr. Christopher Dawson, an extraordinary mentor for young investigators and an eminent scientist in the field of pulmonary physiology, and was very grateful that this book contains one of his last works on the heterogeneity of hypoxic pulmonary vasoconstriction. His presence in the scientific community will be sorely missed.
Christopher A. Dawson, Ph.D., Professor and eminent research scientist died suddenly and unexpectedly on July 12, 2003 at his office. He is recognized as an inspirational mentor, model researcher and has had a profound influence as a teacher and faculty leader at the Medical College of Wisconsin. Dr. Dawson was born in 1942 in Long Beach, California and received his Ph.D. degree from the University of California, Santa Barbara in 1969. As a Professor of Physiology and Medicine at the Medical College of Wisconsin and at Marquette University, he was recognized as one of the world experts in the pulmonary circulation. As documented by more than 200 original research publications and 22 invited reviews and book chapters, he and his associates pioneered many novel technologies that revealed important functions of the lung that were previously unknown. He served as an Associate Editor of the major research journals in his field, Journal of Applied Physiology and American Journal of Physiology. His scholarly and multifaceted works were supported continuously since 1971 by the Department of Veterans Affairs and the National Institutes of Health. Among his many noteworthy discoveries was that the lining of the blood vessels in the lungs contribute critically to the regulation of hormones that modify pulmonary blood flow. He also was instrumental in the first studies to show that isolated small pulmonary arteries contracted and depolarized to hypoxia. His most recent studies using X-ray imaging of the pulmonary circulation have led to a new understanding of how multiple generations of the pulmonary vasculature function under normal and pathological conditions.
His quiet and humble manner, exacting scientific standards and selfless encouragement of other researchers made him a highly sought source of sound advice. Dr. Dawson collaborated closely with a number of bioengineers, physicians, and basic science investigators at Marquette University, the Medical College of Wisconsin, the Zablocki Veterans Hospital, the Froedtert Lutheran Memorial Hospital and the Children's Hospital of Southeast Wisconsin. For his internationally recognized contributions to lung research, Dr. Dawson was given the Medical Career Scientist Award by the Department of Veterans Affairs in 1999, and in the same year he received the Distinguished Service Award by the Medical College of Wisconsin.
Dr. Dawson is survived by his wife Michal Ann, his daughter Marcey Kay and her husband Keith Gulley and their son Dawson Gulley; his son Brian Christopher and wife Cecilia and their daughter Kana Rose; his mother Elvira and father Alfred and his brother Mark and wife Rebecca.
This page intentionally left blank
Was this article helpful?
Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...