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本研究旨在探索在大鼠心肌梗死过程中内源性硫化氢(HS)与一氧化氮(NO)对心肌组织的保护作用和两种气体分子之间的相互作用关系.将试验动物随机分成五组,分别给予HS合成酶胱硫醚-γ-裂解酶(CSE)的抑制剂炔丙基甘氨酸(PAG)和CSE内源性底物左旋半胱氨酸(L-Cysteine),以及NO的合成酶(eNOS)的抑制剂L-NAME和激活剂西地那非(sildenafil),同时设置生理盐水组为对照.给药第七天,建立大鼠心肌梗死动物模型,存活大鼠继续观察48小时.通过对五组试验动物死亡率和心肌梗死面积,血浆中NO和HS的水平,以及心肌组织中CSE酶的活性和CSE和eNOS蛋白水平表达改变和基因水平mRNA的表达变化综合分析,我们认为内源性HS和NO对大鼠心肌梗死均有保护作用,HS-CSE体系和NO-eNOS体系在大鼠心肌梗死过程中呈相互下调的关系趋势.“,”The relationship between hydrogen sulfide (H2S) and nitric oxide (NO) in myocardial infarction (MI) has not been previously reported. In the current investigation, we sought to determine the roles of both H2S and NO in MI in rats. Animals were randomly divided into 5 groups and treated with L-NG-nitro arginine methyl ester (L-NAME), sildenafil, saline, propargylglycine (PAG) and L-cysteine, respectively, for 1 week prior to performing MI surgery or sham operation. The mortality rates were lower in sildenafil and L-cysteine treated rats in the MI group. The infarct area was significantly reduced in sildenafil and L-cysteine treated rats. Moreover, plasma H2S measurements revealed that the level in the sildenafil treated group was lower than in the L-NAME treated MI group, which was consistent with an observed decrease in cystathionine gamma-lyase (CSE) enzyme activity. CSE protein expression level in the L-NAME treated MI group was significantly higher than in sildenafil treated MI group. eNOS protein content in the L-cysteine treated MI group was lower than in the PAG treated MI group and eNOS gene expression is significantly decreased in the L-cysteine treated rats. We demonstrated that endogenous H2S and NO are cardioprotective in the rat model of MI. Indeed, both the H2S-CSE and NO-NOS system appear to have a mutual down-regulation effect in MI process in our experimental rat model.