Enflurane depression of myocardial slow action potentials.

Effects of enflurane on myocardial electrophysiologic and contractile properties were examined by simultaneous measurement of action potentials (APs) and contractions in guinea-pig papillary muscle. Enflurane was administered in 1 to 6% concentrations in 5% CO2-95% O2 bubbled through the standard Tyrode's perfusing solution. After studying normal APs, slow APs were induced with 5 to 30 x 10(-8) M isoproterenol and/or 1 to 2 mM theophylline in partially depolarized muscles (typically -40 mV in 26 mM K+ media). AP characteristics and contractions measured during each enflurane application were analyzed. The maximum rate of rise (+Vmax) and amplitude of the normal AP was not depressed, although duration decreased in greater than or equal to 3% enflurane. In contrast, slow AP + Vmax declined significantly (P less than .05) to 90, 80 and 74% of control in enflurane concentrations of 2, 3 and 4%, respectively. Decrease in slow AP duration was significant only in 5 to 6% enflurane. In 1% enflurane, contractions declined to steady-state levels of 75 (fast AP) and 79% (slow AP) of control and fell to 20 (fast AP) and 35% (slow AP) in 4% enflurane. Enflurane concentrations of 2% and greater inhibit slow (Na+-Ca++) channels which mediate slow APs. This effect may be in part responsible for the negative inotropic effect of enflurane.