It has been proposed that subjects susceptible to high-altitude pulmonary edema (HAPE) show exaggerated hypoxemia with relative hypoventilation during the early period of high-altitude exposure. Some previous studies suggest the relationship between the blunted hypoxic ventilatory response (HVR) and HAPE. To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation (delta VE/delta SaO2). HCVR was measured by the rebreathing method of Read. All measurements were done at Matsumoto, Japan (610 m). All the HAPE-susceptible subjects showed normal values in the pulmonary function test. In HCVR, HAPE-susceptible subjects showed relatively lower S value, but there was no significant difference between the two groups (1.74 +/- 1.16 vs. 2.19 +/- 0.4, P = NS). On the other hand, HAPE-susceptible subjects showed significantly lower HVR than control subjects (-0.42 +/- 0.23 vs. -0.87 +/- 0.29, P less than 0.01). These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. However, values for HVR were within the normal range in 2 of 10 HAPE-susceptible subjects. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contributing factors.
To assess the role of catecholamines in the pathogenesis of high altitude pulmonary edema (HAPE), 24-hour urinary catecholamine excretions and plasma catecholamine concentrations were measured. We also performed brain computed tomography (CT) in the same 8 serial patients with HAPE. 24-hour urinary norepinephrine excretion showeda statistically high value on admission comparedwith that after recovery (396.9±92.9 ug/24 hr, decreasing to 93.0±31.1 ug/24 hr, means±S.E., p <0.01). 24-hour urinary epinephrine excretion on admission was also remarkably high, and returned later normal (62.9± 25.8 ug/24 hr, decreasing to 12.7±4.2 ug/24 hr, p < 0.05). Plasma norepinephrine concentration was also high, but returned to normal (0.260±0.073 ng/ml, to 0.1 1±0.043 ng/ml) by the time of discharge. Brain CT scans revealed diffuse low density of the entire cerebrum, small ventricles, disappearance of sulci, and small cistern, suggesting cerebral edema. These findings may suggest that the heightened sympathoadrenal activity that occurred in the patients concomitant with cerebral edema was related to the high altitude illness rather than to simple exposure to high altitude.
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