硫化氢后处理对大鼠心肌缺血再灌注损伤的保护作用

Protective Effect of Hydrogen Sulfide Postconditioning on Myocardial Ischemia Reperfusion Injury in Rats

【目的】探讨硫化氢后处理对大鼠心肌缺血再灌注损伤的保护作用。【方法】健康成年S-D雄性大鼠30只，随机分成3组，每组10只。假手术组（S组）仅开胸并分离冠状动脉左前降支，但不阻断血流150min；缺血再灌注组（IR组）行冠状动脉左前降支阻断30min，再灌注120min；硫化氢后处理组（H组）于开放左冠状动脉即刻1min内静推硫氢化钠（NartS）0．05mg／kg，再灌注120min。再灌注末抽血测肌钙蛋白I（cTnI），测心肌梗死面积，免疫印迹法测心肌s_腺苷蛋氨酸合成酶（SAM—s）的表达。【结果】和IR组相比，H组心肌梗死面积减小；H组血清中cTnI的含量降低，SAM—S表达降低，且差异均有显著性（P〈0．05）。【结论】硫化氢后处理有心肌保护作用，其机制可能与抑制心肌SAM—S表达有关。

[Objective] To explore the protective effect of hydrogen sulfide（H2 S） postconditioning on my- ocardial ischemia reperfusion injury（I/R） in rats. [Methods]Thirty S-D male rats were randomly assigned to 3 groups with 10 in each. Sham group（group S） only underwent open chest, dissection of left anterior descend- ing coronary artery and perfusion for 150min. Group I/R underwent occulusion of left anterior descending cor- onary artery for 30rain and reperfusion for 120rain. H2 S group（group H） was given the intravenous injection with Naris 0.05mg/kg within 1rain immediately after opening left coronary artery, and the reperfusion for 120rain. Blood samples were taken from arterial line at the end of reperfusion for the determination of plasma troponin（cTnI）. Myocardial infarct size（IS） was measured. Western blotting was used to detect the expression of SAM-s. [Results]Compared with group IR, myocardial infarct size, serum cTnI and SAM-s decreased in group H, and there were significant differences（ P〈0.05）. [Conclusion]H2 S postconditioning has myocardi- al protective effect. It mechanism may be related to the inhibition of the expression of SAM-s in myocardium.