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作 者:赵妍[1] 秦俭[1] 路毅[1] 王晶[1] 邢绣荣[1] 曾翔俊[2] 芦灵巧[2] 孙异临[3]
机构地区:[1]首都医科大学宣武医院急诊科,北京100053 [2]首都医科大学病理生理教研室 [3]北京市神经外科研究所
出 处:《中国急救医学》2006年第12期920-922,共3页Chinese Journal of Critical Care Medicine
基 金:北京市教育委员会科技发展计划项目(No.KM200510025009)
摘 要:目的观察心肺复苏大鼠心肌组织超微结构变化以及乌司他丁(Ulinastatin,UTI)的影响,探讨心肺复苏大鼠心肌损伤的机制及乌司他丁的治疗机制。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(假手术组)、常规复苏组、乌司他丁组,每组8只。于自主循环恢复(ROSC)2h取动脉血,采用酶生化法测定血清中CK-MB的含量;放射免疫法测定血清中TNF-α的含量,采用透射电镜(TEM)观察心肌细胞的损伤情况。结果与常规复苏组比较,乌司他丁组血清中TNF-α的含量显著降低,心功能改善,心肌组织病变减轻。结论大鼠心肺复苏后,血清TNF-α升高参与心肌损伤过程,乌司他丁对复苏后早期的心肌损伤有保护作用。Objective To study the changes of myocardial ultrastructure and effects of Ulinastatin (UTI) on rats after cardiopulmonary resuscitation (CPR) , and to investigate their mechanism. Methods Wistar rats were randomly divided into three groups: sham control group ; routine treatment group; UTI treatment group ( n = 8, per group ). Cardiac arrest was induced by asphyxiation in groups except A and CPR was performed. Two hours after recovery, arterial blood was drew for determination of serum TNF-α and CK - MB. The uhrastructural damages were observed with transmission electron microscope (TEM). Results Compared with routine treatment group, serum level of TNF-α in UTI treatment group decreased significantly and heart function improved. The damage of myocardial ultrastructure was ameliorated markedly. Conclusions TNF-α is probably the extremely important factors that promote the myocardial injury. Ulinastatin can improve the heart function of rats during early stage of resuscitation, and may alleviate the myocardial injury.
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