Abstract: AIM To explore the changes of endogenous H2S during myocardial injury caused by ischemia/reperfusion（I/R）of rat skeletal muscle. METHODS We established the model of bilateral hindlimb I/R in rats by using a tourniquet and 62 Wistar rats were divided into 9 groups at random: group normal (C), group 2 h ischemia (I2), group 4 h ischemia (I4) and groups 4 h ischemia with 0.5 h(R0.5), 2 h(R2), 4 h(R4), 6 h(R6), 12 h(R12), 24 h(R24) reperfusion. The pathologic changes in the myocardium were observed. The levels of plasma H2S, CK-MB and TnT in each group were measured and the CSE activity in myocardium was detected. RESULTS Histopathologic results indicated that myocardial injury was relatively mild after skeletal muscle ischemia but it became much more serious following reperfusion. Compared with that in group normal, the level of plasma CK-MB significantly increased in group I2, and the level of plasma TnT markedly increased in group I4(P<0.05). There were no significant changes in H2S and CSE in ischemia groups. Compared with that in group I4, the level of plasma CK-MB markedly increased in group R0.5(P<0.05), reached peak in group R4 and significantly decreased in group R24. The level of plasma TnT markedly increased in group R4, reached peak in group R6 and still remained at high level in group R4. The level of plasma H2S and the level of myocardial CSE decreased obviously in group R2, R4, R6, R12 (P<0.05) and reached the lowest level in group R4. The level of plasma H2S was negatively correlated with the level of plasma CK-MB (r=-0.78, P<0.05) and TnT (r=-0.89, P<0.05）. CONCLUSION Skeletal muscle ischemia and reperfusion induce myocardial injury. The injury is the most serious in 4-6 hours after reperfusion. The down-regulation of endogenous H2S/CSE system may play an important role in myocardial injury during skeletal muscle IR.