Regulation of delayed afterdepolarizations and aftercontractions in dog ventricular muscle fibres.

Delayed afterdepolarizations have recently been recognized as their important contributions to the genesis of arrhythmias, [3, 6]. This paper deals with the possible causes of the delayed afterdepolarizations and aftercontractions in low K+, high Ca2+ solutions. Simultaneous recordings of membrane potential and tension were employed in dog papillary muscles. The dependence of the amplitude of the delayed afterdepolarizations and the aftercontractions on stimulus frequency and duration of stimulus trains was examined. In addition, effects of isoproterenol, verapamil, caffeine and procaine on both activities were examined. Our results show that conditions causing Ca2+ -overload in the cell provided the development or the augmentation of them. Further, caffeine eliminated oscillatory fluctuations in both activities followed by a transient increase after the treatment and procaine reversibly abolished them. These results support the hypothesis that the delayed afterdepolarizations are caused by a cyclic release of Ca2+ from the sarcoplasmic reticulum under the conditions of Ca2+-overload.