Angiotensin and adrenoceptors in the hemodynamic response to aortic cross-clamping
S. A. Hong, S. Gelman and T. Henderson
Department of Anesthesiology, University of Alabama, Birmingham 35233-1924.
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 alpha 1-adrenergic antagonist (prazosin
hydrochloride, 0.5 mg/kg), a beta-adrenergic antagonist (propranolol
hydrochloride, 5 mg/kg), or an alpha 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 alpha
1-adrenergic antagonist or the angiotensin-converting enzyme inhibitor
developed hypertension of a lesser degree than the control animals, while
rats pretreated with the beta-adrenergic or alpha 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
reninangiotensin and sympathetic nervous systems play an important role in
hemodynamic response to cross-clamping of the thoracic aorta.
