硫化氢预处理延迟相对大鼠心肌缺血-再灌注损伤的保护作用

目的探讨硫化氢预处理延迟相对大鼠心肌缺血-再灌注损伤的保护作用。方法将30只健康成年SD雄性大鼠随机分为三组:假手术组(S组)、缺血-再灌注组(IR组)和硫化氢组(H组)。S组仅开胸并分离冠状动脉左前降支,但不阻断血流150min;IR组行冠状动脉左前降支阻断30min,再灌注120min;H组予以静脉注射NaHS0.05mg/kg,给药后24h同IR组处理。再灌注结束后检测血清超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和心肌梗死面积,电镜观察各组心肌细胞超微结构变化。结果与IR组比较,H组MDA含量降低,SOD活性增高(P<0.05),心肌梗死面积减少(P<0.05),电镜下H组心肌细胞损伤程度减轻。结论硫化氢预处理延迟相对大鼠缺血-再灌注心肌具有保护作用,与抗氧化反应有关。

The protection of hydrogen sulfide delayed preconditioning in rat myocardium after ischemic reperfusion

Objective To investigate the protection of hydrogen sulfide delayed preconditioning on myocardial ischemia reperfusion injury in rats.Methods Thirty Sprague-Dawley male rats were assigned randomly into three groups (n=10 each): group S, control rats that received sham operation; group IR, rats treated with NS (1.0 ml/kg iv) 24 h before ischemia; and group H, rats treated with NaHS (0.05 mg/kg iv) 24 h before ischemia. Group IR and H were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS), the activity of superoxide dismutase(SOD) and the content of malondialdehyde (MDA) in blood were measured. The myocardial ultrastructures were observed under the electron microscopy.Results The IS was significantly reduced in group H (25.40±3.54)% as compared with group IR(38.27±5.64)% (P<0.05). Group H had a lower level of MDA and a higher level of SOD than that of group IR (P<0.05). The degree injury of group H was change better than that of group IR under the electron microscope.Conclusion Hydrogen sulfide delayed preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats by anti-oxidant reaction.