We investigated the relationship between the effects of ischemic preconditi
oning (IPC) and Ca2+ preconditioning (CPC) on reperfusion-induced arrhythmi
as. In the control group (noPC), Langendorff-perfused rat hearts were subje
cted to 5-min zero-flow global ischemia (I) followed by 15-min reperfusion
(I/R), In ischemic preconditioning groups (IPC), the hearts were subjected
to three cycles of 3-min global ischemia and 5-min reperfusion. In the CPC
group, the hearts were exposed to three cycles of 3-min perfusion of higher
Ca2+ (2.3mmol/l Ca2+) followed by 5-min perfusion of normal 1.3mmol/l Ca2, and the hearts were then subjected to I/R. Verapamil was administered in
several hearts of the IPC group (VR+IPC). Ventricular arrhythmias upon repe
rfusion were less frequently seen in the IPC and CPC groups than in the noP
C and VR+IPC groups. IPC and CPC could attenuate conduction delay and enhan
ce shortening of the monophasic action potential duration during ischemia,
The ventricular fibrillation threshold measured at 1-min reperfusion was si
gnificantly higher in the IPC and CPC groups than in the noPC and VR+IPC gr
oups. Verapamil completely abolished the salutary effects of IPC. These res
ults demonstrate that Ca2+ plays an important role in the antiarrhythmic ef
fect of IPC during reperfusion.