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机构地区:[1]南昌大学第二附属医院急诊科,南昌330006
出 处:《中国危重病急救医学》2006年第3期180-183,共4页Chinese Critical Care Medicine
基 金:江西省自然科学基金资助项目(0440083)
摘 要:目的观察眼镜蛇毒因子(CVF)抑制补体激活对创伤失血性休克大鼠血浆内毒素含量的影响。方法80只雄性SD大鼠随机分成对照组和CVF组。建立创伤失血性休克模型,于休克前及复苏后1、6和24 h取血,检测血浆内毒素(LPS)、血清肿瘤坏死因子α(TNFα)含量及血清二胺氧化酶(DAO)和总补体活性(CH 50)。结果对照组大鼠复苏后1 h血CH 50水平迅速下降,血LPS、TNFα水平均明显升高,随后均快速恢复至休克前水平;DAO活性在复苏后1 h和6 h明显升高,然后快速下降。CVF组大鼠除CH 50水平始终<5%,其余各指标复苏后1 h仅略升高,复苏后各时间点均较对照组相应时间点明显降低(P<0.05或P<0.01)。结论在创伤失血性休克中使用补体抑制剂CVF可明显减轻补体激活导致的肠道损伤及肠屏障破坏,减少LPS移位的发生,明显降低血浆LPS含量。Objective To investigate the influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats. Methods Eighty male SD rats were randomly divided into two groups, control and cobra venom factor (CVF) treatment groups. The hemorrhagic shock induced by trauma was replicated in both groups. The animals were killed preshock and at 1, 6, and 24 hours postresuscitation. Twenty - four hours before hemorrhage, rats were given a mainline dose of either 50 μg/kg CVF or an equal volume of saline solution. The plasma and serum samples were collected at each time point to determine the concentration of endotoxin, the activaty of CH50 and diamine oxidase (DAO), and the level of tumor necrosis factor (TNF-α) at various time points in two groups. Results Compared with preshock in control group, serum CH50 levels were decreased promptly at 1 hour postresuscitation. Markedly elevation of the levels of endotoxin and TNF -α in blood were found at early time after resuscitation, and they were come rapidly back to the basic level at 6 and 24 hours phase. The activity of DAO in blood was increased significantly at 1 and 6 hours after resuscitation and declined promptly at 24 hours. Compared with the control group, significantly decline of the levels of endotoxin, TNF-α and DAO at the various time points after resuscitation were also found in the CVF group. The levels of CH50 in CVF group were always less than 5% during the experiment. Conclusion In traumatic hemorrhagic shock rats CVF pretreatment could decline plasma endotoxin levels by preventing the injury of intestine and gut barrier function, decrease endotoxin translocation and reduce plasma endotoxin levels.
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