This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hanaoka, M. Articles by Kubo, K. Search for Related Content PubMed PubMed Citation Articles by Hanaoka, M. Articles by Kubo, K. Related Collections Clinical genetics Other hypertension Pulmonary circulation and disease

(Circulation. 2000;101:1418.)
© 2000 American Heart Association, Inc.

Clinical Investigation and Reports

Hypoxia-Induced Pulmonary Blood Redistribution in Subjects With a History of High-Altitude Pulmonary Edema

Masayuki Hanaoka, MD; Masao Tanaka, MD; Ri-Li Ge, MD; Yunden Droma, MD; Atsuko Ito, MD; Takashige Miyahara, MD; Tomonobu Koizumi, MD; Keisaku Fujimoto, MD; Tadashige Fujii, MD; Toshio Kobayashi, MD; Keishi Kubo, MD

From the First Department of Medicine (M.H., M.T., R.-L.G., Y.D., T.M., T. Koizumi, K.F., T.F., T. Kobayashi, K.K.) and Department of Radiology (A.I.), Shinshu University School of Medicine, Matsumoto, Japan.

Correspondence to Masayuki Hanaoka, MD, First Department of Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. E-mail fountain{at}matsumoto.ne.jp

Background—Pulmonary hypertension has been suggested to play an important role in development of high-altitude pulmonary edema (HAPE), and individual susceptibility has been suggested to be associated with enhanced pulmonary vascular response to hypoxia. We hypothesized that much greater pulmonary vasoconstriction would be induced by acute alveolar hypoxia in HAPE-susceptible (HAPE-s) subjects and that changes in pulmonary blood flow distribution could be demonstrated by radionuclide study.

Methods and Results—We performed ventilation-perfusion scintigraphy in 8 HAPE-s subjects and 5 control subjects while each was in the supine position and acquired functional images of pulmonary blood flow and ventilation under separate normoxic and hypoxic (arterial oxygen saturation, 70%) conditions. We also measured acceleration time/right ventricular ejection time (AcT/RVET) with Doppler echocardiography under each condition in both groups. Moreover, we assayed human leukocyte antigen (HLA) alleles serologically in the HAPE-s group. Pulmonary blood flow was significantly shifted from the basal lung region to the apical lung region under hypoxia in HAPE-s subjects, although no significant change in regional ventilation was observed. With Doppler echocardiography, HAPE-s subjects showed increased pulmonary arterial pressure during hypoxia compared with control subjects. The magnitude of cephalad redistribution of lung blood flow was significantly higher in the HLA-DR6–positive than in HLA-DR6–negative HAPE-s subjects.

Conclusions—These findings suggest that acute hypoxia induces much greater cephalad redistribution of pulmonary blood flow that results from exaggerated vasoconstriction in the basal lung in HAPE-s subjects. Furthermore, pulmonary vascular hyperreactivity to hypoxia may be associated with HLA-DR6.

Key Words: echocardiography • genetics • hypoxia • scintigraphy • vasoconstriction

This article has been cited by other articles:

				T. J. Arai, A. C. Henderson, D. J. Dubowitz, D. L. Levin, P. J. Friedman, R. B. Buxton, G. K. Prisk, and S. R. Hopkins Hypoxic pulmonary vasoconstriction does not contribute to pulmonary blood flow heterogeneity in normoxia in normal supine humans J Appl Physiol, April 1, 2009; 106(4): 1057 - 1064. [Abstract] [Full Text] [PDF]

				E. M. Snyder, K. C. Beck, M. L. Hulsebus, J. F. Breen, E. A. Hoffman, and B. D. Johnson Short-term hypoxic exposure at rest and during exercise reduces lung water in healthy humans J Appl Physiol, December 1, 2006; 101(6): 1623 - 1632. [Abstract] [Full Text] [PDF]

				C. Dehnert, F. Risse, S. Ley, T. A. Kuder, R. Buhmann, M. Puderbach, E. Menold, D. Mereles, H.-U. Kauczor, P. Bartsch, et al. Magnetic Resonance Imaging of Uneven Pulmonary Perfusion in Hypoxia in Humans Am. J. Respir. Crit. Care Med., November 15, 2006; 174(10): 1132 - 1138. [Abstract] [Full Text] [PDF]

				I. R. Starr, W. J. E. Lamm, B. Neradilek, N. Polissar, R. W. Glenny, and M. P. Hlastala Regional hypoxic pulmonary vasoconstriction in prone pigs J Appl Physiol, July 1, 2005; 99(1): 363 - 370. [Abstract] [Full Text] [PDF]

				S. R. Hopkins, J. Garg, D. S. Bolar, J. Balouch, and D. L. Levin Pulmonary Blood Flow Heterogeneity during Hypoxia and High-Altitude Pulmonary Edema Am. J. Respir. Crit. Care Med., January 1, 2005; 171(1): 83 - 87. [Abstract] [Full Text] [PDF]

				M. P. Hlastala, W. J. E. Lamm, A. Karp, N. L. Polissar, I. R. Starr, and R. W. Glenny Spatial distribution of hypoxic pulmonary vasoconstriction in the supine pig J Appl Physiol, May 1, 2004; 96(5): 1589 - 1599. [Abstract] [Full Text] [PDF]

				T Duke Hypoxaemia in developing countries Arch. Dis. Child., April 1, 2003; 88(4): 365 - 365. [Full Text]

				E. R. Swenson, M. Maggiorini, S. Mongovin, J. S. R. Gibbs, I. Greve, H. Mairbaurl, and P. Bartsch Pathogenesis of High-Altitude Pulmonary Edema: Inflammation Is Not an Etiologic Factor JAMA, May 1, 2002; 287(17): 2228 - 2235. [Abstract] [Full Text] [PDF]

				P. Hackett and D. Rennie High-Altitude Pulmonary Edema JAMA, May 1, 2002; 287(17): 2275 - 2278. [Full Text] [PDF]