Key result
Ischemic preconditioning reduces reperfusion ventricular arrhythmias independently of KATP channel blockade in rats.
Why the study?
The mechanisms by which ischemic preconditioning protects against ischemia- and reperfusion-induced arrhythmias, specifically the role of ATP-sensitive potassium channels, were unclear in rats.
May reduce experimental reperfusion arrhythmias via KATP channels; hypothesis-generating and should not yet change clinical practice.
BACKGROUND: Single or multiple brief periods of myocardial ischemic preconditioning (PC) limits ischemia- and reperfusion-induced arrhythmias. This study tested whether PC protects against ischemia/reperfusion-induced arrhythmias and, if so, whether the protective effect was mediated by the opening of ATP-sensitive (KATP) channels. METHODS: In protocol 1, the effects of PC (three cycles of 2 minutes of coronary occlusion and 5 minutes of reperfusion) on the development of arrhythmias after a coronary occlusion of 5, 10, or 20 minutes followed by 10 minutes of reperfusion were studied in rats. In protocol 2, solvent or a KATP channel blocker (glyburide [0.64 mg/kg body weight delivered intravenously]) was administered 5 minutes before PC. In a second group, glyburide was administered immediately after PC. In a third group, solvent, glyburide, or a KATP channel opener (pinacidil [0.16 mg/kg delivered intravenously]) was administered 5 minutes before coronary occlusion for 5 minutes without PC. RESULTS: In protocol 1, PC significantly reduced the ischemia-induced ventricular premature beats (VPBs) and ventricular tachycardia (VT), and it abolished ischemia-induced ventricular fibrillation (VF) during 10 or 20 minutes of coronary artery occlusion. PC also significantly reduced reperfusion-induced ventricular arrhythmias after 5 or 10 minutes of coronary artery occlusion; this effect of PC, however, was lost during reperfusion after 20 minutes of coronary occlusion. In protocol 2, PC again produced a marked reduction in reperfusion-induced arrhythmias and abolished the incidence of VPBs during 5 minutes of ischemia as well as the incidence of irreversible VF during reperfusion, whereas glyburide did not block the protective effect of PC on ischemia- and reperfusion-induced arrhythmias. Glyburide administered in non-PC animals did not reduce ischemia- and reperfusion-induced arrhythmias, nor did pinacidil. CONCLUSIONS: The protective effect of PC was not attenuated by glyburide. These results suggest that the protective effect of PC in ischemia- and reperfusion-induced arrhythmias is not likely to be related to activation of KATP potassium channels during ischemia in rats.
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Lu et al. (1993) studied Myocardial ischemia- and reperfusion-induced arrhythmias. Ischemic preconditioning with or without glyburide vs. Solvent or no preconditioning was evaluated on Ischemia- and reperfusion-induced arrhythmias (ventricular premature beats, ventricular tachycardia, and ventricular fibrillation). Ischemic preconditioning significantly reduced ischemia- and reperfusion-induced ventricular arrhythmias in rats, and this protection was not attenuated by the KATP channel blocker glyburide.
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