Action potential duration is widely used as a measure of refractory period in ischemia. Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of excitability lags behind full repolarization. The purpose the study was to review this phenomenon of postrepolarization refractoriness during ischemia and after application of various antiarrhythmic drugs. The findings showed that although postrepolarization refractoriness is profoundly proarrhythmic during ischemia, it may protect the heart from reentrant arrhythmias in the absence of depolarization of the resting membrane. An increase in postrepolarization refractoriness induced by sodium-channel-blocking drugs may exert an antifibrillatory action.
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