Wong S S, Myerburg R J, Ezrin A M, Gelband H, Bassett A L
Eur J Pharmacol. 1982 Jun 4;80(4):323-9. doi: 10.1016/0014-2999(82)90077-2.
The electrophysiologic effects of encainide were determined in normal and acutely ischemic (30 min) rabbit ventricular muscle cells. Encainide (10(-6), 5 X 10(-6) and 10(-5) M) had no effect on resting potential (RP); 10(-6) M encainide reduced overshoot and action potential (AP) amplitude of cells in normal left ventricles and cells in normal areas of ischemic ventricles. Encainide, 5 X 10(-6) M and 10(-5) M, depressed Vmax and prolonged AP duration of normal cells. Surviving cells within ischemic areas displayed AP with reduced RP, overshoot, AP amplitude, Vmax and shortened AP duration. All encainide concentrations reduced overshoot, AP amplitude and Vmax of depressed AP. Encainide's lengthening of AP duration was greater in cells within ischemic areas than in surrounding normal cells. Encainide (10(-6) M) prolonged effective refractory period and often blocked AP in ischemic cells. Encainide also caused depression in membrane responsiveness. Encainide's differential effect upon AP may significantly contribute to its antiarrhythmic activity in ischemic heart disease.
