Pulmonary hemodynamic responses to hypoxia and exercise in subjects with priorindividuals susceptible to high altitude pulmonary edema. Eldridge, Marlowe W., Andrea Podolsky, Russell S. Richardson, Don H. Johnson, Douglas R. Knight, Emily C. Johnson, Susan R. Hopkins, Hideo Michimata, Bruno Grassi, John Feiner, S. Sadi Kurdak, Philip E. Bickler, Peter D. Wagner, and John W. Severinghaus. Cardiovascular Research Institute and Departments of Pediatrics and Anesthesiology, University of California San Francisco, 1386-HSE Box 0542, San Francisco CA 94143-0542, USA, Department of Medicine, University of California, San Diego, La Jolla, CA. 92093-0623, USA
APStracts 3:0236A, 1996.
Individuals with a prior history ofsusceptible to high altitude pulmonary edema (HAPE-S) appear to have high resting pulmonary arterial pressures, but very little data are available on their vascular responses toduring heavy exercise in this unique population. We studied the We hypothesized that HAPE-S individuals would have an augmented pulmonary vascular response to exercise inthat may explain their predisposition to developing high altitude pulmonary edema (HAPE). We studied 7 healthy HAPE-S people and 9 healthy people controls (CON) with similar altitude experience but no history of HAPE at rest and during graded exercise (35%, 65%, and 85% of maximum) at sea level (SL) and following 2 days at 3810 meters altitude (ALT). At each location studies were conducted with both normoxic (PIO2=148 Torr) and hypoxic (PIO2=91 Torr) gas. studies were conducted. Pulmonary hemodynamic measurements included, Although there was no difference in age, height, weight, oxygen uptake or exercise capacity, forced vital capacity was smaller by 0.9 L (15%) in HAPE-S (p=0.045). We measured cardiac output, and ppulmonary artery (PAP) and occlusion pressures (PAOP), in addition to respiratory and inert gases. A multiple regression analysis demonstrated that the PAP reactivity to exercise was significantly greater in the HAPE-S group. This reactivity was not influenced by altitude or oxygenation, implying that the response was intrinsic to the pulmonary circulation. In contrast PAOP reactivity showed a significant reactivity to exercise was also greater in the HAPE-S group, increasing that was influenced withby altitude but independent ofbut not oxygenation in both study groups. These findings suggestts either an augmented flow-dependent pulmonary vasoconstriction, and/or a reduced vascular cross-sectional area in HAPE-S. HAPE-S demonstrated higher PAP pressures at rest and during exercise at both locations. PAOP was higher in HAPE-S than in CON during exercise with each PIO2 at SL, but at ALT the difference disappeared with both groups demonstrating elevated PAOP. In HAPE-S during SL normoxic peak exercise, 62% of the increase from rest in PAP can be attributed to the high PAOP. At ALT both HAPE-S and CON showed elevated exercise -induced PAOP that contributed more than 50% to the high PAP observed. The high pulmonary vascular pressures that exist both upstream and down stream of the lung must increase mean capillary pressure resulting in enhanced transvascular fluid movement. Our findings therefore suggest that the augmented pulmonary vascular pressures on both sides of the lung may contribute to HAPE-S individuals predisposition to HAPE. 

Received 20 April 1995; accepted in final form 4 April 1996.
APS Manuscript Number A430-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 May 96