EFFECT OF NICORANDIL ON ACUTE MYOCARDIAL INFARCTION AND ARRHYTHMIA INDUCED BY ISOPRENALINE
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Studies on the effect of KATI, channel modulators on cardiac dysfunction and arrhythmia in the setting of myocardial ischemia and reperfusion have been inconsistent. Several studies hypothesized that such agents can preserve myocardial function and decrease infarction size as well as produce antiarrhythmic effect. Other studies have yielded contradictory results, suggesting that non-uniform shortening of the action potential during myocardial ischemia may increase electrical inhomogeneity leading to development of arrhythmia during acute myocardial ischemia with tendency to increase infarct size. The aim of this present study was to assess whether treatment with the KATI, channels opener, nicorandil produces pro- or anti-arrhythmic effect and to find out whether nicorandil given prior to induction of myocardial infarction or during reperfusion results in cardioprotection. Acute myocardial infarction was induced using isoprenaline (300mg/kg. SC) and the effect of pre- and post-infarction treatment with a nonhypotensive dose of nicorandil (03 mg/kg, IV) on ECG, infarct size and CPK enzyme serum level was studied. The results demonstrate that pretreatment with the KATp channel opener. nicorandil administered just prior to induction of infarction offers significant protective effect during ischemia as well as reperfusion in anesthetized rats. Heart rate. T wave voltage. infarction sue and CPI< level were all reduced in the group pretreated with nicorandil prior to the induction of infarction but not the one given nicorandil 39 minutes after the induction of infarction. The protective effect can be regarded as arising out of pharmacological preconditioning and activation of cardiomyocyte mitochondrial KATT, channels. The study provides evidence that nicorandil is not protective when given just prior to the reperfusion.