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为探讨硫化氢(hydrogen sulfide,H2S)对大鼠心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤的保护作用及机制,雄性Sprague-Dawley大鼠被随机分为对照组(假手术组)、I/R组、2.8μmol/kg体重NaHS干预组、14μmol/kg体重NaHS干预组。结扎冠状动脉前降支30min后,松扎再灌注60min,心电图II导联检测和TTC染色测定心肌梗死面积评价制作的心肌I/R模型;测定血浆中H2S浓度变化;监测血流动力学指标(LVSP,LV±dp/dtmax);HE染色和透射电镜观察心肌形态学改变;免疫组织化学方法测定心肌组织中c-Fos蛋白表达。结果显示:心肌I/R后血浆中H2S浓度明显低于对照组[(30.32±5.26)vs(58.28±7.86)μmol/L,P<0.05];2.8和14μmol/kg体重NaHS均可显著改善I/R引起的心功能改变,且14μmol/kg体重NaHS较2.8μmol/kg体重NaHS作用强;14μmol/kg体重NaHS明显减轻心肌形态学及超微结构损伤,同时降低大鼠I/R心肌组织中c-Fos蛋白表达(0.20±0.06vs0.32±0.10,P<0.05)。以上结果提示,H2S对大鼠心肌的I/R损伤有保护作用,这可能与其降低c-Fos蛋白表达有关。
To investigate the protective effect and mechanism of hydrogen sulfide (H2S) on myocardial ischemia / reperfusion (I / R) injury in rats, male Sprague-Dawley rats were randomly divided into control group (sham operation Group), I / R group, NaHS intervention group (2.8μmol / kg body weight) and NaHS intervention group (14μmol / kg body weight). Ligation of the anterior descending coronary artery 30min, reperfusion 60min after reeling, electrocardiogram II lead detection and TTC staining myocardial infarction area evaluation of the production of myocardial I / R model; Determination of plasma H2S concentration changes; monitoring of hemodynamic parameters ( LVSP, LV ± dp / dtmax). The morphological changes of myocardium were observed by HE staining and transmission electron microscopy. The expression of c-Fos protein in myocardium was detected by immunohistochemistry. The results showed that the concentration of H2S in plasma after I / R of myocardium was significantly lower than that in control group [(30.32 ± 5.26) vs (58.28 ± 7.86) μmol / L, P <0.05] / R, and NaHS at 14μmol / kg body weight was stronger than NaHS at 2.8μmol / kg body weight. NaHS at 14μmol / kg body weight significantly reduced myocardial morphological and ultrastructural damage, and at the same time decreased myocardial I / R c-Fos protein expression (0.20 ± 0.06 vs 0.32 ± 0.10, P <0.05). The above results suggest that H2S may have a protective effect on I / R injury in rat myocardium, which may be related to the decrease of c-Fos protein expression.