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Research Article Free access | 10.1172/JCI105513

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.

Address requests for reprints to Dr. David W. Richardson, Dept. of Medicine, Medical College of Virginia, Richmond, Va. 23219.

‡

Recipient of National Heart Institute Research Career Award.

*

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

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.

Find articles by Richardson, D. in: PubMed | Google Scholar

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

†

Occupant of Virginia Heart Association Chair of Cardiovascular Research.

Address requests for reprints to Dr. David W. Richardson, Dept. of Medicine, Medical College of Virginia, Richmond, Va. 23219.

‡

Recipient of National Heart Institute Research Career Award.

*

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

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.

Find articles by Kontos, H. in: PubMed | Google Scholar

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

†

Occupant of Virginia Heart Association Chair of Cardiovascular Research.

Address requests for reprints to Dr. David W. Richardson, Dept. of Medicine, Medical College of Virginia, Richmond, Va. 23219.

‡

Recipient of National Heart Institute Research Career Award.

*

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

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.

Find articles by Raper, A. in: PubMed | Google Scholar

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

†

Occupant of Virginia Heart Association Chair of Cardiovascular Research.

Address requests for reprints to Dr. David W. Richardson, Dept. of Medicine, Medical College of Virginia, Richmond, Va. 23219.

‡

Recipient of National Heart Institute Research Career Award.

*

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

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.

Find articles by Patterson, J. in: PubMed | Google Scholar

Published January 1, 1967 - More info

Published in Volume 46, Issue 1 on January 1, 1967
J Clin Invest. 1967;46(1):77–85. https://doi.org/10.1172/JCI105513.
© 1967 The American Society for Clinical Investigation
Published January 1, 1967 - Version history
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Abstract

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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