Indirect Action of Epinephrine on Intraventricular Conduction Time

In dogs with denervated hearts intravenous infusions of epinephrine (1.0 to 3.0 µg/kg/min) caused marked acceleration of the heart rate and a significant reduction of intraventricular conduction time. Equal doses infused into the descending thoracic aorta increased the heart rate only slightly, but exerted undiminished effects upon conduction time. Evisceration did not modify the intraventricular dromotropic effect of epinephrine so long as the hepatic arterial supply was preserved. Occlusion of the hepatic artery abolished the dromotropic effect of epinephrine without modifying its chronotropic action. The time course of the dromotropic effect and of the kalemic action of epinephrine was approximately the same. Intravenous infusions of KCl matching the hyperkalemic effect of epinephrine caused similar dromotropic actions. Isoproterenol even in high doses (up to 2.0 µg/kg/min) did not decrease intraventricular conduction time and had only a slight hyperkalemic effect. After the administration of SY28 (1.0 mg/kg) epinephrine caused neither hyperkalemia nor decreased intraventricular conduction time. It is concluded that in the heart in situ the effect of epinephrine on intraventricular conduction is the result of an indirect action mediated through the liberation of K + ions from the liver.