Hemodynamic and sympathoadrenal responses to altitude in humans: effect of dexamethasone

Abstract

Altitude exposure alters hemodynamics and sympathoadrenal function and elicits acute mountain sickness (AMS). Since dexamethasone prevents AMS and influences responsiveness to catecholamines, we studied hemodynamic and sympathoadrenal responses to 4,570 m simulated altitude in 8 subjects treated with dexamethasone or placebo. Mean pulse rates were less at altitude with dexamethasone (96.1 for placebo and 84.1 for dexamethasone; treatment-altitude interaction, p = 0.0045). Altitude led to a postural decline in mean arterial pressure (posture-altitude interaction, p = 0.0026), but this was not affected by dexamethasone. Dexamethasone reduced urinary epinephrine to a greater extent during altitude exposure (from 9.41 ng.mg-1 creatinine with placebo to 4.16 with dexamethasone) when compared with sea level (from 3.24 to 3.08). Urinary excretion of norepinephrine was unchanged at altitude. We conclude that acute altitude exposure is associated with stimulation of the adrenal medulla and not the sympathetic nervous system. Dexamethasone blocks the adrenal medullary response and blunts the pulse rate increase at altitude.