摘要：AbstractThe prevention of myocardial damage occurring from ischemia/reperfusion (IR) is a major issue in ischemic heart disease in civilized worldwide. The object of recent study was based on investigating the anti-arrhythmogenic effect of quercetin postconditioning (QPC) in IR injury in rats, aiming at the involvement of nitric oxide (NO) system and mitochondrial K-ATP (mitoKATP) channels activities. Upon separation of the hearts of 64 male Wistar rats, they were randomly assigned to eight groups (n = 8/group). Except for the sham group, ischemia has exerted by inducing interruption of the aortic supply for 30 min ischemic condition, then 55 min reperfusion. Each experiment lasted 100 min in total with 15 min as stabilization period. The levels of LDH in coronary effluent were estimated colorimetrically. Overall the experiment lambeth convention-based used to assess arrhythmias, which were classified as number and severity of premature ventricular complexes (PVC), number and duration of ventricular fibrillation (VF), and ventricular tachycardia (VT). The arrhythmias induced by IR, LDH and number and duration VF significantly enhanced in control group (P < 0.05 vs. control). The Que group could reduce the LDH level, number of PVC, number and duration of VT, VF and severity of arrhythmias (P < 0.05 compared with control). The effects of Que were abrogated by the concurrent administration of L-NAME (L-nitro-arginine methyl ester) or 5-HD (5-hydroxydecanoate) as selective antagonists of NO system and mitoKATPchannel, respectively. Accumulating evidence indicates that the cardioprotective effect of QPC highlights the importance of in anti-arrhythmogenic during IR, thereby opening a new direction for treatment in patients with myocardial infarction (MI).
