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Electrophysiologic effects of encainide on acutely ischemic rabbit myocardial cells
Abstract:
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.
Insights
Encainide affects cardiac cells differently in normal and ischemic conditions. This drug alters action potential characteristics, potentially contributing to its antiarrhythmic effects in ischemic heart disease.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Acute ischemia significantly alters cardiac cell electrophysiology.
- Understanding drug effects on both normal and ischemic cells is crucial for antiarrhythmic therapy.
Purpose of the Study:
- To investigate the electrophysiologic effects of encainide on normal and acutely ischemic rabbit ventricular muscle cells.
- To determine if encainide's effects differ between normal and ischemic cardiac tissue.
Main Methods:
- Rabbit ventricular muscle cells were exposed to varying concentrations of encainide (10^-6 M, 5 X 10^-6 M, 10^-5 M).
- Electrophysiologic parameters including resting potential, action potential amplitude, Vmax, and action potential duration were measured.
- Cells from both normal and acutely ischemic (30 min) left ventricles were studied.
Main Results:
- Encainide did not affect resting potential but reduced action potential amplitude and Vmax in a dose-dependent manner.
- Action potential duration was prolonged by encainide, with a greater effect observed in ischemic cells.
- Encainide also prolonged the effective refractory period and sometimes blocked action potentials in ischemic cells, while depressing membrane responsiveness.
Conclusions:
- Encainide exhibits differential electrophysiologic effects on normal and ischemic cardiac cells.
- The drug's ability to modulate action potential characteristics in ischemic tissue may underlie its antiarrhythmic properties in ischemic heart disease.