RESUMEN
Objective To explore the effects and mechanism of hydrogen sulfide on myocardial ischemia reperfusion in rats. Methods With sodium hydrogen sulfide (NaHS) as a donor of hydrogen sulfide ( H2S), we established myocardial ischemia-reperfusion injury model in rats. The SD rats were randomly divided into control group,myocardial ischemia reperfusion group (I/R group), H2S group,and H2S and glibenclamide (H2S + GLI)group. We monitored the hemodynamics index of rats, including heart rate, arterial pressure, left ventricular pressure. The rate of ventrical arrhythmia was also observed in each group. Results H2 S significantly reduced the ventricular arrhythmia (VA) occurrence (H2S group 66.5% vs I/R group 33.5% (P ＜0.05) and score in myocardial ischemia reperfusion rats (H2S group 2. 6 ±0. 7 vs I/R group 4. 5 ±0. 8(P＜0.05). The KATP channel blocker,glibenclamide,could weaken the antiarrhythmic effects of H2S ( H2S group 2. 6 ±0. 7 vs. H2S + GLI group 4. 0 ± 0. 6, P ＜ 0.05 ). Conclusions H2S has the protective effect against myocardial ischemia reperfusion damage. This function may be associated with the KATP signal transduction pathway in cells.