The calcium paradox: an electrophysiological study in the isolated rabbit heart

In Langendorff perfused rabbit heart (37 degrees C) transmembrane potentials were recorded from the left ventricle with 'floating' microelectrodes. During calcium-free perfusion, action potential duration lengthened by 55.4 +/- 34.9% (n = 8). AV conduction time increased, until Wenckebach and 2 : 1 AV block occurred. Heart rate initially decreased, and later increased although control values were not reached. Upon reperfusion with normal calcium-containing fluid, a few vigorous contractions occurred, which dislodged the intracellular microelectrode. As far as could be established, cells depolarized within 6-60s to values less than -50 mV, and no action potentials could be recorded. During low-calcium (50 mumol l-1) perfusion (n = 5), action potential duration initially increased, but later decreased. When perfusion with normal calcium-containing fluid was resumed when action potentials were still longer than normal, the action potentials shortened initially but returned later to control values. In these hearts, contractions reappeared. However, when perfusion with normal calcium-containing fluid was resumed when action potential duration was shorter than normal, no contractions reappeared, and action potentials remained short during the entire reperfusion period. In six experiments, creatine kinase release was determined during both low-calcium and calcium-free perfusion, and during subsequent periods with normal calcium-containing fluid. During 10 min of low-calcium perfusion, 107 +/- 31 IU g-1 dry weight appeared in the perfusate, and in the subsequent normal calcium perfusion period of 15 min, 438 +/- 88 IU were released. During the 10 min calcium-free period, 141 +/- 40 IU were released, and during 15 min of reperfusion, 2773 +/- 258 IU appeared.(ABSTRACT TRUNCATED AT 250 WORDS)