Some Factors Influencing Potentiation of Cardiac Contractility Following an Extrasystolic Beat.

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Abstract
Using isolated quiescent rabbit auricles, the effect of an extrasystole, introduced at controlled intervals, was to increase the contractility, i.e., potentiate the post-extra-systolic beat. The effect of increasing the stimulus intensity of the extrasystolic beat on the production of the post-extra-systolic potentiation (PEP) was to reduce the minimal interval and raise the PEP to a maximal height at that minimal interval. As the minimal interval for extrasystole production and maximal PEP appeared related to the effective refractory period, the variations in this property were studied for their effect on potentiation. Rate changes and quinidine salfate were used to vary the refractory period. At very low rates (0.2-0.5/second), PEP was minimal or absent. Increasing rates (0.5-5.0/second) produced a rise in both basal and post-extrasystolic contractility (greater in the latter) up to 3/second with a marked reduction in both above this rate. Addition of quinidine sulfate increased the effective refractory period and decreased both basal and post-extrasystolic contractility; the latter more than the former. Possible mechanisms of post-extrasystolic potentiation (PEP) and the occurrence of PEP in intact, blood perfused hearts are discussed.

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