Hypoxia-induced pulmonary blood redistribution in subjects with a history of high-altitude pulmonary edema

Background-Pulmonary hypertension has been suggested to play an important r ole 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 v asoconstriction would be induced by acute alveolar hypoxia in HAPE-suscepti ble (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 HA PE-s subjects and 5 control subjects while each was in the supine position and acquired functional images of pulmonary blood flow and ventilation unde r separate normoxic and hypoxic (arterial oxygen saturation, 70%) condition s. We also measured acceleration time/right ventricular ejection time (AcT/ RVET) with Doppler echocardiography under each condition in both groups. Mo reover, we assayed human leukocyte antigen (HLA) alleles serologically in t he HAPE-s group. Pulmonary blood flow was significantly shifted from the ba sal 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 arteri al pressure during hypoxia compared with control subjects. The magnitude of cephalad redistribution of lung blood flow was significantly higher in the HLA-DRG-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 exaggerat ed vasoconstriction in the basal lung in HAPE-s subjects. Furthermore, pulm onary vascular hyperreactivity to hypoxia may be associated with HLA-DR6.