Protection by the calcium antagonist tiapamil, against cardiac lymphatic enzyme leakage and arrhythmias in canine hearts during reperfusion.

We examined the effects of tiapamil, a Ca2+ antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca2+ channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion.