鈥� 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 伪1-adrenergic antagonist (prazosin hydrochloride, 0.5 mg/kg), a 尾-adrenergic antagonist (propranolol hydrochloride, 5 mg/kg), or an 伪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 伪1-adrenergic antagonist or the angiotensin-converting enzyme inhibitor developed hypertension of a lesser degree than the control animals, while rats pretreated with the 尾-adrenergic or 伪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)