Role of sarcoplasmic reticulum in digitalis-induced electrical and mechanical oscillations in the heart.

The mechanism of cardiac oscillatory activity induced by digitalis was studied in the canine ventricular muscle. We determined the role of sarcoplasmic reticulum in the phenomenon of oscillatory afterpotential and mechanical aftercontractions. Additionally we wished to study the interaction between changes in stimulus interval, which are known to affect sarcoplasmic reticulum function and these oscillatory phenomena. Aftercontraction was induced by ouabagenin but it required previous stimulation of the heart. The production of aftercontraction depended on short stimulus interval and bore no relation with the size of the releasable pool of Ca in the sarcoplasmic reticulum as indicated by the size of the driven contraction. Aftercontraction was often seen without an accompanying action potential. When a depolarization was present during aftercontraction, its temporal relation with the contraction often did not show the usual delay, suggesting that electrical activity may not necessarily initiate contraction. This was supported by the finding that Mn, a Ca channel blocker, blocked normal contractions more than aftercontraction. However, inhibition of Ca release from the sarcoplasmic reticulum by ryanodine or of Ca reuptake by caffeine were effective in blocking aftercontraction and when present, oscillatory afterpotential. Abolition of aftercontraction was not due to slowing of relaxation. These studies confirm the role of sarcoplasmic reticulum in causing aftercontraction and oscillatory afterpotential during ouabagenin toxicity and also suggest that there is a relationship between the 'repriming' ability of the sarcoplasmic reticulum and the oscillatory phenomena.