Do pronethalol, disopyramide, and quinidine have similar antifibrillatory actions and effects on intracellular cardiac potentials in rabbit isolated atria?
Pronethalol, disopyramide, and quinidine share similar electrophysiological effects on rabbit atria, supporting the view that interference with depolarization is essential for antifibrillatory activity.
A quantitative comparison of the effects of quinidine, pronethalol and gamma-di-isopropylamino-alpha-phenyl-alpha-pyrid-2-ylbutyramide (disopyramide) has been made on rabbit isolated atria. All three drugs raised the electrical threshold and reduced the contractions, the conduction velocity and the maximal frequency at which the atria would follow a stimulus. The descending order of potency was pronethalol, quinidine and disopyramide, but the range was small, pronethalol having about twice the activity of disopyramide. Both the new compounds affected intracellular potentials in the same way as quinidine, causing little change in the resting potential or duration of the action potential, but reducing the overshoot potential and slowing the rate of rise of the action potential. These results support the view that interference with depolarization is an essential feature of antifibrillatory activity.
Sekiya et al. (Sun,) studied this question.