脓毒症大鼠心肌氧化应激损伤及心肌细胞超微结构变化  

Myocardial oxidative stress injury and myocardial ultrastructure in septic rats

作　　者：白静[1] 张文丽[2] 张军伟[1] 程爱斌[1] 李志强[1] 王红阳[3] 

机构地区：[1]河北联合大学附属医院重症医学科,河北唐山063000 [2]河北联合大学医学实验研究中心,河北唐山063000 [3]河北联合大学附属医院呼吸内科,河北唐山063000

出　　处：《细胞与分子免疫学杂志》2015年第5期634-638,共5页Chinese Journal of Cellular and Molecular Immunology

基　　金：河北省医学科学研究重点课题(20140238)

摘　　要：目的探讨盲肠结扎穿孔致脓毒症大鼠心肌损伤的机制。方法健康雄性SD大鼠54只,随机分为正常组、假手术组、脓毒症组。采用盲肠结扎加穿孔(CLP)法建立脓毒症模型,分别在术后3、6、12、24 h(每个时间点6只大鼠)测定各组血清肌钙蛋白I(c Tn I)、一氧化氮(NO),以及心肌组织超氧化物歧化酶(SOD)、丙二醛(MDA)水平,HE染色观察心肌病理学改变,透射电镜观察心肌细胞超微结构变化。结果正常组、假手术组大鼠相比,脓毒症组大鼠血清c Tn I、NO、心肌组织MDA水平显著升高,SOD显著降低,心肌细胞水肿,炎细胞浸润,间质血管扩张充血,并可见局灶性心肌坏死;电镜下肌原纤维排列紊乱,闰盘间隙增宽,线粒体空泡化。结论脓毒症大鼠心肌损害与氧化应激损伤有关,随着病程的进展,心肌细胞超微结构的损害加重。Objective To investigate the mechanism of myocardial injury in septic rats by cecal Ugation and puncture. Methods Fifty-four male Sprague-Dawley （SD） rats were randomly divided into 3 groups： normal group （n = 6）, sham group （n=24）, sepsis group （n =24）. Cecal ligation and puncture （CLP） was adopted to reproduce animal models of sepsis. The contents of cardiac troponin I （cTnl） and nitric oxide （NO） in serum and the activities of superoxide dismutase （SOD） and malondialdehyde （MDA） in myocardium were detected in each group 3, 6, 12, 24 hours after the operation （with 6 rats at each time point）. The changes of myocardial pathomorphology were observed by HE staining under a microscope. The ultrastructurel changes of myocardial cells were observed by the electron microscopy. Results The levels of serum cTnl and NO in the sepsis group were much higher than those in the sham group and the normal group. At the same time, the activity of MDA in myocardium in the sepsis group was also significantly higher than that in the other two groups. While the activity of SOD was obviously lower. Besides, uitrastructural changes in sepsis ones included myocardial cell edema, inflammatory cell infiltration, interstitial angiectasis and hyperemia and visible focal myocardial necrosis. Myocardial cell injury was more serious in sepsis rats compared with the other two groups. Electron microscopy showed different degrees of disorganized myofibrils, widened intercalated disc gap, decreased mitochondrial cristae and vacuolation of myocardium in sepsis group. Conclusion The myocardial cell injury is due to oxidative stress injury in septic rats. As the disease progresses, the myocardial ultrastructure damage becomes worse gradually.

关 键 词：脓毒症 心肌损伤 氧化应激 超微结构 

分 类 号：R574[医药卫生—消化系统] R541[医药卫生—内科学]