Membrane current changes induced by acetylstrophanthidin in cardiac Purkinje fibers.

Voltage clamp experiments were carried out with short Purkinje fibers exposed to acetylstrophanthidin. A consistent change in membrane current was an appearance of a transient inward current on repolarization to the resting potential from the preceding depolarization, when preparations were treated with sufficient concentration of acetylstrophanthidin to cause the transient depolarization. This transient inward current displayed voltage- and time-dependence on the preceding depolarization, of which kinetics were different from the pacemaker K+ current. The transient inward current was easily blocked by manganese ions. The results indicated that acetylstrophanthidin induced the transient inward current which was the basis of the transient depolarization and the current might represent an abnormal state of the slow inward current possibly related to the altered internal Na+ and Ca++ concentrations.