钙敏感受体在大鼠心肌缺血/再灌注损伤中的作用

目的观察钙敏感受体在大鼠心肌缺血/再灌注损伤中的作用及其机制。方法30只Wistar大鼠随机分为3组(每组10只):假手术组(sham组)、缺血/再灌注组(I/R组)和钙敏感受体激动剂组(Gdcl3组),采用冠状动脉结扎和松结的方法,制备大鼠在体心肌缺血/再灌注损伤模型。分别测定血清一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)水平,光镜及透射电镜下观察心肌结构病理变化。结果I/R组血清LDH、MDA水平明显高于sham组(P<0.01),NO、SOD低于sham组(P<0..01);Gdcl3组血清LDH、MDA水平明显高于I/R组(P<0.01),而NO、SOD低于I/R组(P<0.01)。光镜及透射电镜下可观察到Gdcl3组心肌结构破坏,心肌细胞呈灶状或片状坏死;线粒体损伤,核皱缩,核染色质边集,其病理学改变程度较I/R组严重。结论钙敏感受体激活可使氧自由基产生增加,减少NO含量,降低SOD活性,加重心肌缺血/再灌注损伤。

Effect of calcium sensing receptor on myocardial ischemia/reperfusion injury in rats

Objective To observe the effect of calcium sensing receptor(CaSR) on myocardial ischemia/reperfusion(I/R) injury in rats and to explore the underlying mechanism.Methods Thirty Wistar rats were randomly divided into 3 groups:sham group,I/R group and calcimimetic group(Gdcl_3 group).The rat myocardial I/R injury model was established by ligating and then reperfusing the left descending coronary artery(LAD).The levels of serum nitric oxide(NO),malondialdehyde(MDA),superoxide dismutase(SOD) and lactate dehydrogenase(LDH) were measured.The pathological I/R changes in the myocardium were evaluated by light microscopy and electron microscopy.Results In I/R group,there was significant increase in the levels of serum MDA and LDH as well as decrease in the level of serum NO and SOD activity compared to sham group.Significant increase in serum MDA and LDH level and decrease in serum NO and SOD activity were observed in Gdcl_3 group in comparison to I/R group.In Gdcl_3 group,there were patchy necrosis of muscle fibers with neutrophil infiltration,myofilament disruption,mitochondria damage,nucleus shrinkage and chromatic margination,indicating that myocardial damage of Gdcl_3 group was more severe than I/R group.Conclusion CaSR activation may be partly associated with the myocardial ischemia/reperfusion injury by increasing oxidative damage.