alpha 1-adrenoceptor stimulation is able to reverse halothane-induced cardiac depression in isolated rat hearts.

Abstract

Stimulation of myocardial alpha 1-adrenoceptors has been shown to exert positive inotropic effects through a cyclic AMP-independent mechanism. The purpose of this study was to examine if alpha 1-adrenoceptor stimulation is able to attenuate myocardial depression produced by exposure to halothane, and to test if alpha 1-adrenoceptor stimulation alters myocardial oxygen supply-demand balance in hearts exposed to halothane. The effects of phenylephrine were examined in 7 isolated perfused rat hearts. Variables measured were: heart rate, isovolumetric peak left ventricular pressure (LVP), LV dP/dt, coronary arterial flow, myocardial O2 delivery (DO2), myocardial O2 consumption (MVO2) and the ratio of DO2/MVO2. Each heart was exposed to phenylephrine cumulatively 0.1 microM, 0.3 microM, 1 microM and 3 microM under the administration of 1% halothane in the presence of propranolol 1 microM. Halothane 1% decreased the heart rate by 9 +/- 3%, LVP by 37 +/- 3%, and LV dP/dt by 35 +/- 2%. Phenylephrine restored these decreases to the baseline levels. Phenylephrine maintained or further enhanced the reductions in coronary flow and DO2 produced by halothane, resulting in a decrease in the DO2/ MVO2 ratio. alpha 1-adrenoceptor stimulation is capable of restoring direct cardiac depressant effects of halothane with a possible impairment of the oxygen supply-demand balance.