摘要
目的:观察乌司他丁对重症肺炎大鼠心肌损伤的保护作用及其机制研究。方法:60只大鼠随机分为对照组、鲍曼组及鲍曼+乌司他丁组,各20只。鲍曼组及鲍曼+乌司他丁组大鼠麻醉后行气管插管,沿导管壁滴入100μL鲍曼不动杆菌,对照组滴入等量生理盐水,之后鲍曼+乌司他丁组大鼠腹腔注射乌司他丁(10万U/kg,1次/d),连续3 d,对照组及模型组注射等量生理盐水。72 h后,用心功能分析系统记录大鼠心功能变化;综合应用病理学及分子生物学方法观察大鼠心肌变化。结果:与对照组比,鲍曼组大鼠心功能下降,血清cTNI、CK-MB、BNP含量升高,肺组织及心肌组织病理损伤较重(P<0.01)。与鲍曼组相比,鲍曼+乌司他丁组大鼠LVEDP水平下降,LVDP、+dP/dtmax、-dP/dtmax水平明显升高;血清cTNI、CK-MB、BNP水平降低幅度分别为36.3%、24.5%、29.9%;肺组织及心肌组织病理损伤减轻;鲍曼组的MMP数值为0.653,鲍曼+乌司他丁组的MMP数值为0.821,较鲍曼组升高25.7%;心肌凋亡蛋白Bcl-2上升,Caspase-3表达降低(P<0.05)。结论:乌司他丁对重症肺炎大鼠心肌损伤具有较好的保护作用,其机制可能与减轻线粒体损伤及细胞凋亡有关。
Objective: To observe the protective effect of Ulinastatin on myocardial injury in rats with severe pneumonia and to explor its mechanism. Methods: 60 rats were randomly divided into Control group, Baumannii group and Baumannii + Ulinastatin group,20 in each group. The rats in Baumannii group and Baumannii + Ulinastatin group were anesthetized and intubated. 100 μL Acinetobacter baumannii(AB) was drip along the catheter wall. The Control group was drip with equal amount of saline. Ulinastatin was administered intraperitoneally at a dose of 100,000 U/kg daily to mice in Baumannii + Ulinastatin group for 3 days, whereas the Control group and Baumannii group received 0.9% saline. We use cardiac function analysis system to record the changes in rat heart function 72 hours later;myocardial changes were observed by means of pathology and molecular biology. Results: Compared with Control group, the cardiac function, the level of cTNI, CK-MB and BNP in serum, as well as lung tissue and myocardial tissue pathological damage were severe in Baumannii group(P <0.01). Compared with Baumannii group, the level of LVEDP in Baumannii + Ulinastatin group was decreased, and the levels of LVDP,+ dP/dtmax and-dP/dtmax were increased significantly. The pathological changes of lung tissue and myocardial tissue were alleviate, this cardioprotective effect was also seen in increased mitochondrial membrane potential(MMP) level,The MMP value in Baumannii group was 0.653, and the MMP value in Baumannii + Ulinastatin group was 0.821, which was 25.7 %higher than that of Baumannii group;The decreasement level of serum cTNI, CK-MB, and BNP were 36.3%, 24.5%, and 29.9% respectively. Besides, the expression of apoptosis related protein Bcl-2 was increased and Caspase-3 was significantly decreased with Ulinastatin treatment(P<0.05). Conclusions: Ulinastatin play protective effect on myocardial injury in rats with severe pneumonia. Its mechanism may be related to the reduction of mitochondrial injury and apoptosis.
作者
赵品
赵敏
杨倩
高龙飞
胡晓亮
蒯建科
ZHAO Pin;ZHAO Min;YANG Qian;GAO Long-fei;HU Xiao-liang;KUAI Jian-ke(Department of Anesthesiology,Xi'an No.3 Hospital,the Affiliated Hospital ofNorthwest Uniwersity,Xi'an,Shaanxi,710018,P.R. China)
出处
《现代生物医学进展》
CAS
2019年第18期3443-3448,共6页
Progress in Modern Biomedicine
基金
陕西省科研基金项目（2018SF-095）
关键词
重症肺炎
心肌损伤
线粒体损伤
凋亡
乌司他丁
Severe pneumonia
Myocardial injury
Mitochondrial damage
Apoptosis
Ulinastatin
