Effects of transmembrane potential on oscillatory afterpotentials induced by acetylstrophanthidin in canine ventricular tissues.

Transmembrane activity was recorded from isolated canine false tendons or trabeculae by using standard differential microelectrode techniques. Exposure of the tissues to acetylstrophanthidin (AS; 0.5-2 X 10(-7) g/ml) induced oscillatory afterpotentials in false tendons but not in muscle. When the transmembrane potential of the isolated tissues was altered by externally applied current, progressive depolarization of false tendons caused the amplitude of oscillatory afterpotentials to increase to a maximum and then decrease. Hyperpolarization abolished oscillatory afterpotentials and unmasked activity attributable to the normal pacemaker mechanism. Any level of manifest oscillatory afterpotential-related toxicity, including phasic decreases in excitability, could be elicited by careful selection of membrane potential. The effects of the imposed membrane potentials were immediately reversed with the return of membrane potential to control levels. In muscle, exposed to AS but not exhibiting oscillatory afterpotentials, depolarization revealed oscillatory afterpotentials. In both false tendons and muscle, depolarization to membrane potentials of -50 mV or less before exposure to AS elicited depolarization-induced automaticity. Subsequent exposure of the tissues to AS abolished this activity. This study demonstrates an important role of membrane potential in digitalis toxicity.