Use of drugs at high altitude

Abstract

I T is important to determine if drugs frequently employed in aviation medicine act differently at high altitudes. Modification of action under such conditions might occur because of diminished barometric pressure, partial anoxia or extreme cold. Various attempts have been made to use drugs to improve altitude tolerance and to relieve the pain of decompression sickness. Evidence is lacking that many substances actually increase altitude tolerance. It is unlikely that any drug will be more than moderately effective so far as intensity or duration of action is concerned. During the war emphasis was placed, almost certainly correctly, on improvements in oxygen equipment rather than on temporary and uncertain measures designed to enable men to get along with unsatisfactory equipment. Various dietary factors have been given considerable attention in the belief that such measures would be more lasting and physiologic. It is suggested from studies of visual’ and psychomotor2 performance that the ingestion of large amounts of glucose will improve performance under hypoxic conditions. There is some evidence that a low blood sugar interferes with oxygenation of the central nervous system314 so that a simultaneous mild hypoxia and hypoglycemia produce symptoms similar to those associated with severe oxygen lack and normal blood sugar. This may be justification for supplying foods rich in carbohydrate to personnel immediately before they fly to high altitudes.5 Experimentally 50 Gm. or more of glucose has been employed with moderate improvement in performance. l Some time ago it was reported that animals on a carrot diet were more resistant to the lethal effects of hypoxia than animals on an ordinary diet. 617 This has been confirmed* but when a loss of reflex response or electroencephalograms were used as criteria9 no improvement was noted. So far no dietary factor other than glucose has been demonstrated to be of definite value. Experimentally, subconvulsive doses of apomorphine, camphor, tetrazol, potassium cyanide and strychnine have all been shown to protect against the lethal effects of anoxia in mice but the respiratory stimulating effect may have been the most important factor.“’ Under similar conditions full narcotic doses of ethyl alcohol are effective, perhaps through a general reduction in metabolism with a subsequent diminution in oxygen requirement. l1 Anesthetic doses of amytal or of pentobarbital sodium were not beneficial but moderate doseP of diphenylhydantoin sodium gave some protection. Further studies of agents affecting the autonomic nervous system13 revealed that cholinergic and sympathicolytic drugs protected against the lethal effects of acute anoxia in mice but adrenergic agents increased the lethal effects. In general, drugs which increase the metabolic rate, such as thyroxine and dinitrophenol, l4 diminish hypoxia tolerance. Several studies have shown that the adrenal cortex is involved in some manner with tolerance to oxygen deficiency.15’16 During the initial phase of anoxia the blood sugar is normal and the amount of glycogen stored in the liver is diminished. This may result from an increased utilization of carbohydrate. Further adaptation to anoxia involves increased protein catabolism with a rise in carbohydrate stores and an increase