ACTIONS OF PHENYLEPHRINE, ISOPROTERENOL, AND EPINEPHRINE WITH HALOTHANE ON ENDOCARDIAL CONDUCTION AND ACTIVATION IN CANINE LEFT-VENTRICULARPAPILLARY-MUSCLES

Background: Myocardial sensitization by halothane to the arrhythmogeni c effects of epinephrine involves synergistic actions mediated by alph a(1)-and beta-adrenoceptors. Halothane potentiates a transient a(1)-ad renoceptor-mediated negative dromotropic effect of epinephrine on Purk inje fibers. This study examines hom halothane alters the actions of a lpha(1)-and beta-agonists and epinephrine on endocardial conduction. M ethods: Superfused canine papillary muscles were mapped to locate a Pu rkinje-ventricular muscle junction (PVJ), and bipolar electrodes were placed to measure Purkinje and endocardial conduction velocity and PVJ conduction time during stimulation of the Purkinje layer. The effects of exposure to 5 mu M phenylephrine, 1 mu M isoproterenol, or 5 mu M epinephrine on conduction mere determined in the absence and presence of 0.4 mM halothane in three groups of 10 preparations. Results: Isopr oterenol slightly increased Purkinje conduction velocity and markedly improved conduction at the Per and in the endocardium similarly in the presence or absence of halothane. Phenylephrine depressed Purkinje ve locity (-12%) only in the presence of halothane and did not slow condu ction at the PVJ or in the myocardium. Epinephrine transiently depress ed Purkinje velocity, more so with (-22%) than without (-12%) halothan e (P less than or equal to 0.01), and simultaneously facilitated condu ction at the PVJ and in the myocardium. Conclusions: The prodysrhythmi c actions of epinephrine With halothane may involve disparate effects on conduction, including speeding of conduction at the PVJ and in the myocardium, similar to that produced by isoproterenol, accompanied by simultaneous but transient alpha(1)-mediated depression of conduction in the Purkinje system.