THE PROTECTION BY ISCHEMIC PRECONDITIONING AGAINST MYOCARDIAL ISCHEMIA-INDUCED AND REPERFUSION-INDUCED ARRHYTHMIAS IS NOT MEDIATED BY ATP-SENSITIVE POTASSIUM CHANNELS IN RATS

Background: Single or multiple brief periods of myocardial ischemic pr econditioning (PC) limits ischemia- and reperfusion-induced arrhythmia s. This study tested whether PC protects against ischemia/reperfusion- induced arrhythmias and, if so, whether the protective effect was medi ated by the opening of ATP-sensitive (K(ATP)) channels. Methods: In pr otocol 1, the effects of PC (three cycles of 2 minutes of coronary occ lusion and 5 minutes of reperfusion) on the development of arrhythmias after a coronary occlusion of 5, 10, or 20 minutes followed by 10 min utes of reperfusion were studied in rats. In protocol 2, solvent or a K(ATP) channel blocker (glyburide [0.64 mg/kg body weight delivered in travenously]) was administered 5 minutes before PC. In a second group, glyburide was administered immediately after PC. In a third group, so lvent, glyburide, or a K(ATP) channel opener (pinacidil [0.1 6 mg/kg d elivered intravenously]) was administered 5 minutes before coronary oc clusion for 5 minutes without PC. Results: In protocol 1, PC significa ntly reduced the ischemia-induced ventricular premature beats (VPBs) a nd ventricular tachycardia (VT), and it abolished ischemia-induced ven tricular fibrillation (VF) during 10 or 20 minutes of coronary artery occlusion. PC also significantly reduced reperfusion-induced ventricul ar arrhythmias after 5 or 10 minutes of coronary artery occlusion; thi s effect of PC, however, was lost during reperfusion after 20 minutes of coronary occlusion. In protocol 2, PC again produced a marked reduc tion in reperfusion-induced arrhythmias and abolished the incidence of VPBs during 5 minutes of ischemia as well as the incidence of irrever sible VF during reperfusion, whereas glyburide did not block the prote ctive effect of PC on ischemia- and reperfusion-induced arrhythmias. G lyburide administered in non-PC animals did not reduce ischemia- and r eperfusion-induced arrhythmias, nor did pinacidil. Conclusions: The pr otective effect of PC was not attenuated by glyburide. These results s uggest that the protective effect of PC in ischemia- and reperfusion-i nduced arrhythmias is not likely to be related to activation of K(ATP) potassium channels during ischemia in rats.