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Address requests for reprints to Dr. David W. Richardson, Dept. of Medicine, Medical College of Virginia, Richmond, Va. 23219.
Supported by grant DA MD 49-193-65-9153 from the U. S. Army Research and Development Command. Office of the Surgeon General. Department of the Army, and in part by grants H-3361. HTS-5573, and FR 00016-02 from the National Institutes of Health.
In 17 healthy men, beta-adrenergic blockade reduced significantly the tachycardia and the elevation of cardiac output associated with inhalation of 7.5% oxygen for 7 to 10 minutes.
Hypoxia did not increase plasma concentrations of epinephrine or norepinephrine in six subjects. Furthermore, blockade of alpha and beta receptors in the forearm did not modify the vasodilation in the forearm induced by hypoxia, providing pharmacologic evidence that hypoxia of the degree and duration used was not associated with an increase in the concentrations of circulating catecholamines in man.
Part of the increase in cardiac output and heart rate during acute hypoxia in man is produced by stimulation of beta-adrenergic receptors, probably by cardiac sympathetic nerves. The mechanism of the vasodilation in the forearm during hypoxia remains uncertain.