The electrophysiologic effects of encainide were determined in normal and acutely ischemic (30 min) rabbit ventricular muscle cells. Encainide (10-6, 5 × 10-5 M) had no effect on resting potential (RP); 10-6 encainide reduced overshoot and action potential (AP) amplitude of cells in normal left ventricles and cells in normal areas of ischemic ventricles. Encainide, 5 × 10-6 M and 10-5M, depressed V̇max and prolonged AP duration of normalcells. Surviving cells within ischemic areas displayed AP with reduced RP, overshoot, AP amplitude, V̇max and shorterned AP duration. All encainide concentrations reduced overshoot, AP amplitude and V̇max 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 AP in ischematic cells. Encanides also caused depression in membrane responsiveness. Encainide's differential effect upon AP may significantly contribute to its antiarrhythmic activity in ischemic heart disease.
- Action potential
- Effective refractory period
- Membrane responsiveness
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience