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

OBJECTIVE

To investigate the effects of ischemic preconditioning (PC) and ATP sensitive K+ channels (KATP(+) opener nicorandil on reperfusion arrhythmias and electrophysiology.

METHODS

Langendorff-perfused rat hearts were subjected to ischemic PC with three cycles of 2 minutes of global ischemia or infusion of KATP(+) opener nicorandil with subsequent 5 minutes global ischemia and reperfusion. The incidence of reperfusion arrhythmias, ventricular fibrillation threshold (VFT), effective refractory period (ERP) and monophasic action potential duration (MAPD) of the left and right ventricles were compared to those from control rat hearts.

RESULTS

The results indicated that PC reduced the incidence of total arrhythmias and ventricular fibrillation during reperfusion (P < 0.05, vs controls). 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. KATP+ opener nicorandil neither reduced the incidence of total arrhythmias and VF nor delayed arrhythmia onset. Nicorandil shortened ERP and MAPD90 without enhancing the VFT values, and VFT returned to normal as slowly as that in controls.

CONCLUSIONS

We conclude that PC protects the globally ischemic rat hearts from reperfusion arrhythmias. The antiarrhythmic effect of PC is likely to be related to a significant increase of VFT. KATP(+) opener nicorandil has no potential antiarrhythmic action and KATP(+) channels may not play a major role in the antiarrhythmic effects of ischemic PC in isolated rat hearts.