The increased sympathoadrenal activity in patients with high altitude pulmonary edema is centrally mediated.

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Abstract
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 showed a statistically high value on admission compared with 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 0.11±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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