补体激活对创伤失血性休克大鼠血浆内毒素含量的影响

Influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats

目的观察补体激活对创伤失血性休克大鼠血浆内毒素含量的影响。方法雄性SD大鼠建立创伤失血性休克模型，随机分成对照组和眼镜蛇毒因子（CVF）组，根据观察时间点的不同各组再分为休克前，复苏后1、6、24h时相组。结果对照组大鼠复苏后1h血CH50水平迅速下降，血LPS浓度、TNF—α水平均明显升高，随后二个时间点快速恢复至休克前水平；DAO活性在复苏后1h和6h明显升高，然后快速下降。CVF组大鼠除CH50水平始终〈5％．其余各指标复苏后1h仅略升高，其复苏后各时相组均较埘照组相应时相组明显降低。结论创伤失血性休克大鼠补体早期激活，其可能通过损伤肠道使内毒素移位导致血浆LPS含量增加。

Objective To investigate the influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats. Methods Eighty of male SD rats were randomly divided into two groups： control and cobra venom factor （CVF） treatment groups. In each group, the animals were killed at serial time points： preshock and at 1, 6, and 24 hours postresuscitation. Twenty four hours before hemorrhage, rats were given an mainline dose of either 50μg/kg CVF or an equal volume of saline solution. To imitate the clinic process, this experiment establishes an animal model of common clinic traumatic hemorrhagenic shock. The plasma and serum samples were collected to determine the concentration of endotoxin, the activaty of CH50 and DAO, and the level of 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 h. 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 complement activation occurred early, it might cause the injure of gut, make gut barrier function damaged, and result in endotoxin translocation.