α1-adrenoceptor stimulation is able to reverse halothaneinduced cardiac depression in isolated rat hearts

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 1μM.
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: α₁adrenoceptor stimulation is capable of restoring direct cardiac depressant effects of halothane with a possible impairment of the oxygen supply-demand balance.     

Effects of phenylephrine and prostaglandin E on ventriculo-arterial matching during halothane anaesthesia

We have investigated the effects of phenylephrine alone andcombined with prostaglandin E₁ (PGE₁) on ventriculo-arterialmatching during halothane anaesthesia in dogs. The ratio ofleft ventricular end-systolic elastance (Ees) to effective arterialelastance (Ea) was used as an index of ventriculo-arterial matching.In group 1 (n = 7), measurements were performed at control,1.5% halothane, halothane+phenylephrine 1–10 µgkg^–1 min^–1, and halothane + phenylephrine + PGE₁,0.2–1.0 or 1.0–2.0 µg kg^–1 min^–1.In group 2 (n = 5), dobutamine 2 and 5 µg kg^–1 min^–1was infused during halothane anaesthesia. Halothane 1.5% decreasedmean arterial pressure (MAP), cardiac output and Ees. Phenylephrinerestored MAP, but further decreased cardiac output. The decreasein Ees produced by halothane was reversed by phenylephrine.PGE₁ increased cardiac output and reversed the increases inEa and Ea/Ees during phenylephrine infusion. Dobutamine alsoreversed halothane-induced decreases in MAP, cardiac outputand Ees, and improved Ea/Ees. Our results indicate that combineduse of PGE₁ with phenylephrine can eliminate the vasoconstrictiveproperty of phenylephrine, resulting in an improvement in ventriculo-arterialmatching.