Drug Use at High Terrestrial Altitudes and in Cold Climates: A Brief Review

Acetazolamide, methazolamide, and spironolactone taken prophylactically generally produce a reduction in the occurrence of symptoms of Acute Mountain Sickness (AMS), but are not a panacea. Such prophylactic use may indirectly improve exercise performance due to the alleviation of A M S symptoms. Dexamethasone, phenytoin, and furosemide effectiveness remains uncertain, and more controlled studies are indicated. Antacids apparently provide no relief from AMS. Valium is contraindicated at altitude because it produces mind altering effects at a time when preservation of mental competence is critical. A report claiming the usefulness of nifedipine in treating High A ltitude Pulmonary Edema (HAPE) during a mountain climb warrants further investigation. Partial alleviation of the presumably synergestic cold-air and exercise-induced asthma can be achieved in many so afflicted by premedication with cromolyn sodium or its combination with terbutaline sulphate. Attempts to use thyroid hormone or triiodothyronine for the stimulation of heat production and peripheral vasodilators for increasing skin and other peripheral temperatures in order to prevent cold injury to tissue have thus far yielded inconclusive results

Calorigenic Effect of Norepinephrine Correlated with Plasma Free Fatty Acid Turnover and Oxidation *

The increase in oxygen consumption caused by administration of epinephrine has been extensively studied in animals and in man. Many physiological and biochemical correlations have been made and many different hypotheses have been advanced to explain this so-called calorigenic effect, but there is still no clearly established consensus regarding the mechanism or mechanisms involved (1, 2). In recent years it has become clear that one of the most striking metabolic effects of the catecholamines is their ability to stimulate mobilization of depot fat in the form of free fatty acids (FFA) (3). Studies by Fritz, Davis, Holtrop, and Dundee (4) and by Eaton and Steinberg (5) have shown, moreover, that the rate of oxidation of labeled FFA by isolated skeletal muscle preparations in vitro is a function of the concentration of FFA in the medium. Similar effects of FFA concentration on FFA oxidation have been demonstrated in rat liver slices (6) and in perfused rat liver (7). We have previously suggested, therefore, that the calorigenic action of catecholamines might be due, at least in part, to their effect in mobilizing FFA (5). The present clinical studies were undertaken to explore this possibility further. Because the metabolic effects of epinephrine are somewhat more complex than those of norepinephrine, in that the former actively mobilizes glucose as well as FFA, the present studies were done primarily with norepinephrine. It is shown that infusion of norepinephrine increases the rate of oxyge