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Amendment history:
  • Errata (April 1969)

Free access | 10.1172/JCI105700

Vascular responses after alpha adrenergic receptor blockade: II. Responses of venous and arterial segments to adrenergic stimulation in the forelimb of dog

Francois M. Abboud and John W. Eckstein

Cardiovascular Research Laboratories, Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa

Find articles by Abboud, F. in: PubMed | Google Scholar

Cardiovascular Research Laboratories, Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa

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

Published January 1, 1968 - More info

Published in Volume 47, Issue 1 on January 1, 1968
J Clin Invest. 1968;47(1):10–19. https://doi.org/10.1172/JCI105700.
© 1968 The American Society for Clinical Investigation
Published January 1, 1968 - Version history
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Abstract

The effects of nerve stimulation and of intraarterial injections of norepinephrine on arterial and venous resistances were studied in the perfused forelimb of dog before and after administration of the alpha adrenergic receptor blocker phenoxybenzamine.

Pressures were recorded from the perfused brachial artery and a small metacarpal vein in the forepaw. Blood flow to the whole forelimb was maintained constant. Changes in perfusion pressure in the brachial artery reflected primarily changes in arterial resistance and changes in small vein pressure reflected changes in resistance of venous segments downstream from the point of pressure measurement.

Alpha receptor blockade reduced vasoconstrictor responses to both nerve stimulation and norepinephrine. Responses to angiotensin, used in these experiments as an internal control, were not blocked consistently in a dose-related manner indicating that the effects of phenoxybenzamine were specific to adrenergic stimuli.

Increases in venous pressure in response to norepinephrine and to nerve stimulation were blocked almost completely whereas increases in arterial pressure were reduced only in part by the blocker. The more effective reduction of pressor responses in the small vein was not caused by a passive reduction in blood flow through the paw nor was it caused by a reduction in the concentration of norepinephrine in the venous effluent reaching the venous segments.

This differential effect of alpha receptor blockade on increases in venous and arterial resistances may account for the beneficial effect of phenoxybenzamine in shock.

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