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Modification by Beta-Adrenergic Blockade of the Circulatory Responses to Acute Hypoxia in Man*

David W. Richardson, Hermes A. Kontos, A. Jarrell Raper and John L. Patterson, Jr.

Department of Medicine, Medical College of Virginia, Richmond, Va.

Occupant of Virginia Heart Association Chair of Cardiovascular Research.

Recipient of National Heart Institute Research Career Award.

* Submitted for publication January 10, 1966; accepted September 22, 1966.

Published January 1967

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.

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