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目的研究心搏骤停大鼠心肺复苏早期应用乌司他丁(Ulinastatin,UTI)对自主循环恢复后2 h 心肌氧自由基、血清CKMB、TNFα及大鼠心肌超微结构的影响。方法利用窒息导致大鼠心脏骤停后心肺复苏的动物模型,将 Wistar 大鼠随机分为3组:对照组、常规复苏组、UTI 治疗组,每组8只。于自主循环恢复2 h 取动脉血,测定血清中 CK-MB、TNFα的含量;取心肌组织,制备心肌匀浆测 NO、MDA 含量及 SOD 的活性。采用透射电镜观察心肌细胞的超微结构。结果常规复苏组与对照组比较,血清TNFα明显升高(P<0.01),血清 CKMB、心肌 MDA,NO 有升高趋势,SOD 活性降低.电镜下对照组心肌细胞超微结构正常,常规复苏组心肌细胞部分线粒体外膜不完整,线粒体嵴模糊不清,有肿胀;乌司他丁组各项指标检测结果较常规复苏组好,电镜下可见细胞线粒体增生,线粒体嵴结构正常。结论心肺复苏大鼠存在心肌损伤,乌司他丁组 CK-MB、TNFα、自由基以及心肌超微结构均较常规复苏组有改善,对复苏后心肌损伤有一定的保护作用。
Objective To investigate the effects of Ulinastatin (UTI) on myocardial oxygen free radicals, serum CKMB, TNFα and myocardium ultrastructure in rats after cardiopulmonary arrest 2 h after spontaneous circulation recovery. Methods Wistar rats were randomly divided into 3 groups: control group, routine resuscitation group and UTI treatment group, 8 rats in each group. The animal model of cardiopulmonary resuscitation after cardiac arrest was induced by asphyxia. The arterial blood was recovered 2 hours after spontaneous circulation and the contents of CK-MB and TNFα in serum were determined. The myocardial tissues were taken out to measure the content of NO and MDA and the activity of SOD in myocardium homogenate. Transmission electron microscopy was used to observe the ultrastructure of cardiomyocytes. Results Compared with the control group, the levels of TNFα, CKMB, MDA and NO in serum of normal resuscitation group were significantly increased (P <0.01), and the activity of SOD was decreased. The ultrastructure of myocardial cells was normal in control group and normal resuscitation group Myocardial cell mitochondrial outer membrane incomplete, mitochondrial cristae blurred, swelling; ulinastatin group of indicators of the test results than the conventional recovery group, under electron microscopy, mitochondria proliferation, mitochondrial cristae structure is normal. Conclusion Myocardial injury was observed in CPR rats. The levels of CK-MB, TNFα, free radicals and myocardial ultrastructure were improved in the ulinastatin group compared with those in the conventional revascularization group, and had a protective effect on myocardial injury after CPR.