Effect of calcium on digitalis induced transient depolarizations in dog Purkinje tissue

Transmembrane activity was recorded from isolated canine false tendons exposed to acetylstrophantidin (AS). Concentrations from 1 to 2x10^-7 g/ml caused transient depolarization (TD) coupled to driven action potentials at a time when slow diastolic depolarization was depressed. TD could reach threshold and induce extrasystoles and complex arrhythmias. TD were abolished by Mn (2 mM) or by reduction of [Ca]. Elevation of [Ca] increased the amplitude and rate of rise of TD. High [Ca] (12.5 mM) caused TD and depression of phase four depolarization in the absence of AS. Elevation of [K] depressed and reduction of [K] potentiated TD caused by either AS or high [Ca]. The results indicate TD and arrhythmias produced by AS may be caused by a transient Ca influx.