Postextrasystolic potentiation of contraction is directly related to the prematurity of the extrasystole and decays over several beats, independent of changes in action potential configuration or fiber potassium content.
The phenomenon of postextrasystolic potentiation of contraction has been studied in papillary muscles isolated from the right ventricle of dog and cat hearts. Isometric tension has been recorded by means of an electronic transducer (RCA #5734) and electrical activity of single fibers by means of an intracellular microelectrode. The degree of potentiation of contraction resulting from a single extrasystole is directly related to the degree of prematurity of this beat. Evidence has been obtained which indicates that the potentiation is maximally effective immediately after the extrasystole and decays at a progressively slower rate during the course of seven to ten beats. The appearance of postextrasystolic potentiation is not dependent upon the changes in frequency of contraction, diastolic interval or presystolic tension which result from the premature contraction. Studies of the transmembrane potentials of single fibers reveal no change in amplitude and little change in configuration of the action potentials associated with potentiated beats. Studies of the resting transmembrane potential and the effects of changes in extracellular concentrations of K and Ca fail to support the concept that potentiation is related solely to changes in the fiber K content. It is concluded that postextrasystolic potentiation results from mechanisms which remain unknown.
Hoffman et al. (1956) studied this question.