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目的研究牛磺酸对渐增再灌注处理的离体大鼠缺血/再灌注损伤心肌的保护作用。方法采用Langendorff离体心脏灌流法制备离体大鼠心肌缺血/再灌注模型。SD大鼠随机分为7组:正常对照组(Nor)、缺血/再灌注组(I/R)、渐增再灌注组(GR)、牛磺酸低浓度组(T20)、牛磺酸高浓度组(T40)、渐增再灌注联合牛磺酸低浓度组(GT20)、渐增再灌注联合牛磺酸高浓度组(GT40)。记录平衡末及再灌注90min心功能,TTC染色法测定心肌梗死面积,检测冠脉流出液中乳酸脱氢酶(LDH)活性及心肌组织中Caspase-3活性,TUNEL法检测心肌细胞凋亡。结果与缺血/再灌注组比较,GR、牛磺酸能够改善心功能,减少心肌梗死面积,减少LDH漏出,降低心肌Caspase-3活性并减少心肌细胞凋亡;相比单纯应用GR及牛磺酸,渐增再灌注联合牛磺酸的保护作用更强,且GT40组保护作用最强。结论 GR和牛磺酸均能减轻大鼠离体缺血/再灌注心肌的损伤,牛磺酸,特别是高浓度牛磺酸能够增强渐增再灌注对心肌的保护作用,抗凋亡可能是二者发挥心肌保护作用的机制之一。
Objective To study the protective effect of taurine on myocardial ischemia / reperfusion injury induced by increasing reperfusion in isolated rat hearts. Methods The isolated myocardial ischemia / reperfusion model was induced by Langendorff perfusion in vitro. SD rats were randomly divided into 7 groups: normal control group (I / R), ischemia / reperfusion group (GR), taurine low concentration group (T20) High concentration group (T40), increasing reperfusion combined with taurine low concentration group (GT20), increasing reperfusion combined with taurine high concentration group (GT40). Cardiac function was recorded at the end of the balance and 90 min after reperfusion. The area of myocardial infarction was determined by TTC staining. The activity of lactate dehydrogenase (LDH) and the activity of Caspase-3 in myocardium were measured by enzyme-linked immunosorbent assay. Cardiomyocyte apoptosis was detected by TUNEL assay. Results Compared with ischemia / reperfusion group, GR and taurine could improve cardiac function, decrease myocardial infarct size, decrease LDH leakage, decrease myocardial Caspase-3 activity and decrease cardiomyocyte apoptosis. Compared with GR and taurine Acid, increasing reperfusion combined with taurine stronger protective effect, and GT40 group the strongest protective effect. Conclusion Both GR and taurine can attenuate the myocardial ischemia / reperfusion injury in rats. Taurine, especially high concentration of taurine, can enhance the protective effect of increasing reperfusion on myocardium. One of the mechanisms by which cardioprotection is exerted.