CATECHOLAMINES, HYPOXIA AND HIGH-ALTITUDE

Hypoxia is a potent activator of the sympathetic nervous system by sti mulating arterial chemoreceptors. However, out of 15 laboratory studie s on the effects of acute and prolonged hypoxia on catecholamines, 14 failed to show any changes in plasma or urinary noradrenaline and only four studies showed significant increases in plasma or urinary adrena line. By contrast, six out of eight studies on MSNA showed increased s ympathetic nerve activity to the leg. An increased clearance of plasma catecholamines during hypoxia may be a possible explanation. Furtherm ore, many of the studies had limitations in a number of subjects and c atecholamine assays used. Emotional aspects of the study protocols, wh ich could contribute to the increase in adrenaline, was only assessed by sham runs in one chamber study. However, 13 out of 14 reviewed fiel d studies on subjects staying for more than 1 week at high altitude, r eported increased plasma or urinary excretion of noradrenaline which m ay be compatible with increased sympathetic activity. Adrenaline chang ed to a lesser degree. Out of seven studies on more short-term (4 h to 3 days) exposure to high altitude, only one demonstrated significantl y increased plasma noradrenaline. In this study, however, several subj ects had been exposed to high altitude less than 1 week before the exp eriment. In a new study on 12 climbers reported in this paper, a tempo rary reduction in plasma catecholamines was found 2 days after arrival at 4200 m. There was a steady increase towards normal levels after 1 week. Plasma vasopressin (AVP) increased suggesting a compensatory mec hanism. Both plasma noradrenaline and adrenaline were positively corre lated with oxygen saturation in these subjects. Thus, in previously un acclimatized subjects, short-term exposure to high altitude does not i ncrease plasma catecholamines, rather plasma levels decreased. In addi tion to increased clearance, there is some evidence of reduced synthes is of catecholamines during short-term hypoxia. The oxygen sensitivity of tyrosine hydroxylase (TH) activity, may be one possible mechanism.