Comparison of the Effects of Nicorandil and Sodium Nitroprusside on the Progression of Microvascular Obstruction in the Myocardial Infarction Zone in Rats.

Recent studies have shown that exogenous nitric oxide alleviates tissue injury caused by ischemia and reperfusion. The multitarget drug nicorandil possessing a dual mechanism of action combining the release of nitric oxide with opening of ATP-dependent K channels seems promising. We studied the infarction-limiting effect of nicorandil and its impact on the progression of the no-reflow/slow flow phenomenon in the myocardial infarction zone in rats compared to sodium nitroprusside. In a rat in vivo model of regional myocardial ischemia and reperfusion, neither nicorandil nor sodium nitroprusside reduced myocardial infarction size in rats with early no-reflow. Despite the dual mechanism of action of nicorandil (0.2 mg/kg), sodium nitroprusside (60 μg/kg) was more effective in reducing the size of the early no-reflow zone, and a trend toward a decrease in the no-reflow zone was observed at the end of 2‑h reperfusion.