Background. Stimulation of myocardial α1-adrenoceptors has been shown to exert positive inotropic effects through a cyclic AMP-independent mechanism. The purpose of this study was to examine if α1-adrenoceptor stimulation is able to attenuate myocardial depression produced by exposure to halothane, and to test if α1-adrenoceptor stimulation alters myocardial oxygen supply-demand balance in hearts exposed to halothane. Methods. 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 μM, 0.3 μM, 1 μM and 3 μM under the administration of 1% halothane in the presence of propranolol 1 μM. Results. 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. Conclusion. α1-adrenoceptor stimulation is capable of restoring direct cardiac depressant effects of halothane with a possible impairment of the oxygen supply-demand balance.
|Number of pages||6|
|Journal||Acta Anaesthesiologica Scandinavica|
|Publication status||Published - Jan 1 1997|
All Science Journal Classification (ASJC) codes
- Anesthesiology and Pain Medicine