Abstract
Comment: This sophisticated, detailed, and meticulously worked laboratory report furnishes further data on the intracellular mechanisms of action of halothane and isoflurane in preparations of rat thoracic aorta smooth muscle strips and the interactions of calcium and calcium channel blockers (in this case, verapamil). Previous studies on the interaction of verapamil with volatile anesthetics suggested that verapamil abolished the decrease in cardiac output induced by low calcium and exaggerated the increase in stroke volume and left ventricular contractility induced by high levels of calcium.1 The effects of calcium channel blockers when used in combination with enflurane were also studied and were an exaggeration of the reduction of cardiac output and stroke volume induced by hypocalcemia. Other studies comparing the combination of nifedipine and volatile anesthetics found the prime interaction to be with enflurane, causing an exaggerated reduction in atrial rate and contractility unaccompanied by any effects on atrioventricular conduction.2 The impact of verapamil on enflurane was not examined in this study. The clinical implications regarding the use of calcium channel blockers in the presence of volatile anesthetics from these in vivo and in vitro studies are, as yet, unclear.
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