Effects of ischemic preconditioning on reperfusion arrhythmias and electrophysiology in isolated rat hearts: it is not a role of K-ATP(+) channels

Objective To investigate the effects of ischemic preconditioning (PC) and A TP sensitive K+ channels (K-ATP(+)) opener nicorandil on reperfusion arrhyt hmias and electrophysiology. Methods Langendorff-perfused rat hearts were subjected to ischemic PC with three cycles of 2 minutes of global ischemia or infusion of K-ATP(+) Opener nicorandil with subsequent 5 minutes global ischemia and reperfusion. The incidence of reperfusion arrhythmias, ventricular fibrillation threshold (V FT), effective refractory period (ERP) and monophasic action potential dura tion (MAPD) of the left and right ventricles were compared to those from co ntrol rat hearts. Results The results indicated that PC reduced the incidence of total arrhyt hmias and ventricular fibrillation during reperfusion (P < 0.05, vs control s). PC markedly delayed the onset of arrhythmia after reperfusion (P < 0.01 , vs controls). PC significantly enhanced the VFT values during reperfusion and shortened the ERP and the MAPD during ischemia. VFT was restored more rapidly than that in controls. K-ATP(+) Opener nicorandil neither reduced t he? incidence of total arrhythmias and VF nor delayed arrhythmia onset. Nic orandil shortened ERP and MAPD(90) without enhancing the VFT values, and VF T returned to normal as slowly as that in controls. Conclusions We conclude that PC protects the globally ischemic rat hearts f rom reperfusion arrhythmias. The antiarrhythmic effect of PC is likely to b e related to a significant increase of VFT. K-ATP(+) opener nicorandil has no potential antiarrhythmic action and K-ATP(+) channels may not play a maj or role in the antiarrhythmic effects of ischemic PC in isolated rat hearts .