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. |
