Nicorandil Improves Post-Ischemic Myocardial Dysfunction in Association With Opening the Mitochondrial KATP Channels and Decreasing Hydroxyl Radicals in Isolated Rat Hearts

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Background Nicorandil has been reported to induce cardioprotection by opening the mitochondrial KATP channels. However, whether nicorandil affects reactive oxygen species is unclear. Methods and Results The hearts of male Sprague-Dawley rats were excised and perfused on a Langendorff apparatus with Krebs-Henseleit solution with a gas mixture of 95% O_2 and 5% CO_2. 1 mmol/L of nicorandil was given 10 min before ischemia. Left ventricular developed pressure (LVDP, mmHg), ±dP/dt (mmHg/s) and coronary flow (ml/min) were continuously monitored. All hearts were perfused for a total of 120min consisting of a 30min pre-ischemic period, followed by a 30min global ischemia and 60min reperfusion with and without 5-hydroxydecanoic acid sodium salt (5-HD), a mitochondrial KATP channel blocker. The concentrations of 2,3-dihydroxybenzoic acid (2,3-DHBA), an indicator of hydroxyl radicals, in the perfusate during reperfusion period were also measured. Nicorandil significantly improved LVDP and ±dP/dt, and increased coronary flow during reperfusion. Pretreatment with 5-HD abolished the improvement of LVDP and ±dP/dt, and the increase in coronary flow induced by nicorandil. Nicorandil significantly attenuated the concentrations of 2,3-DHBA during reperfusion, which were restored by 5-HD. Conclusion Nicorandil is protective against post-ischemic left ventricular dysfunction in association with opening the mitochondrial KATP channels, decreasing hydroxyl radicals and increasing coronary flow in the isolated rat heart.
社団法人日本循環器学会の論文
2006-11-20

Nicorandil Improves Post-Ischemic Myocardial Dysfunction in Association With Opening the Mitochondrial KATP Channels and Decreasing Hydroxyl Radicals in Isolated Rat Hearts

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