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Angiotensin and Adrenoceptors in the Hemodynamic Response to Aortic Cross-clamping
Sun-Ae Hahm Hong, MD;
Simon Gelman, MD, PhD;
Todd Henderson
Arch Surg. 1992;127(4):438-441.
Abstract
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This study was designed to test the hypothesis that activation of adrenoceptors and/or the renin-angiotensin system plays an important role in the overall hemodynamic response to aortic cross-clamping. The experiments were performed on anesthetized rats pretreated with either saline (control group), an angiotensin-converting enzyme inhibitor (enalapril maleate, 2 mg/kg), an 1-adrenergic antagonist (prazosin hydrochloride, 0.5 mg/kg), a β-adrenergic antagonist (propranolol hydrochloride, 5 mg/kg), or an 2-adrenergic antagonist (atipamezole, 5 mg/kg). Cross-clamping of the thoracic aorta was associated with an expected increase in mean arterial pressure and systemic vascular resistance in all animals. During the period of cross-clamping, cardiac output gradually decreased in all groups. Animals pretreated with the 1-adrenergic antagonist or the angiotensin-converting enzyme inhibitor developed hypertension of a lesser degree than the control animals, while rats pretreated with the β-adrenergic or 2-adrenergic antagonist demonstrated a greater arterial hypertension than the control animals. The possible mechanisms underlying the observed differences are discussed. In conclusion, the present study confirms the posed hypothesis that the renin-angiotensin and sympathetic nervous systems play an important role in hemodynamic response to cross-clamping of the thoracic aorta.
(Arch Surg. 1992;127:438-441)
Author Affiliations
From the Department of Anesthesiology, The University of Alabama at Birmingham.
Footnotes
Accepted for publication November 9, 1991.
Reprint requests to Department of Anesthesiology, The University of Alabama at Birmingham, 169 S 19th St, Birmingham, AL 35233-1924 (Dr Gelman).
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