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眼镜蛇毒因子对创伤失血性休克大鼠肠道的作用 被引量:1

Effect on intestine by cobra venom factor in traumatic hemorrhagic shock rats
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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肠道的影响。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、24 h时相组。结果对照组大鼠复苏后1 h血总补体活性(CH_(50))水平迅速下降,血内毒素(LPS)浓度、肠黏膜损伤评分均明显升高,随后2个时间点快速恢复至休克前水平;二胺氧化酶(DAO)活性在随后1 h和6 h时相明显升高,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,其复苏后各时相组均较对照组相应时相组明显降低。结论在创伤失血性休克中使用补体抑制剂可明显减轻补体激活导致的肠道损伤及肠屏障破坏,减少内毒素移位的发生,明显降低血浆内毒素含量。 Objective To investigate the influence of cobra venom factor on the change of intestinal mucosa in traumatic hemorrhagic shock rats. Method An animal model of common clinic traumatic hemorrhagenic shock was established. Male SD rats were randomly divided into two groups: control and CVF groups. In each group, the animals were killed at various time points : preshock and at 1, 6 and 24 hours postresuscitation, Results Compared with preshock in control group, serum CH50 level was decreased promptly at 1 hour postresuscitation, the levels of LPS and histologic injury scoring of intestinal tissue were increased markedly at 1 hour postresuscitation, and they were rapidly back to the basic level at 2 hours phase. The activity of DAO in blood was increased significantly at 1 boar and 6 boors after resuscitation and declined promptly at 24 hours. Compared with preshock in CVF group, the levels of LPS and DAO in blood were increased mildly at early phase after resuscitation. Compared with the control group, the results of the various time point after resuscitation were declined significantly. The levels of CH50 in CVF group were always less than 5% during the experiment. Conclusions In traumatic hemorrhagic shock rats, complement inhibitor could prevent the injury of intestine and gut barrier function caused by complement activation, decrease endotoxin translocation and decline plasma endotoxin levels.
出处 《中华急诊医学杂志》 CAS CSCD 2007年第6期567-571,共5页 Chinese Journal of Emergency Medicine
基金 江西省自然科学基金(0440083)
关键词 创伤失血性休克 二胺氧化酶 眼镜蛇毒因子 内毒素移位 肠道损伤 Traumatic hemorrhagic shock Diamine oxidase Cobra venom factor Endotoxin translocation Intestinal injury
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  • 1盛志勇,姚咏明.脓毒症与多器官功能障碍综合征[J].中华急诊医学杂志,2003,12(10):653-654. 被引量:78
  • 2Hassoun HT, Kone BC, Mercer DW, et al. Post-injury multiple organ failure: the role of the gut [J]. Shock, 2001, 15 (1): 1-10.
  • 3Fruchterman TM, Spin DA, Wilson MA, et al. Complement inhibition prevents gut ischemia and endothelial cell dysfunction after hemorrhage/ resuscitation [J]. Surgery, 1998, 124 (9): 782-792.
  • 4Han XB, Liu X, Hsueh W, et al. Macrophage inflammatory protein-2 mediates the bowel injury induced by platelet-activating factor [J]. Am J Physiol Gastrointest Liver Physiol, 2004, 287 (6) : 1220-1226.
  • 5Durham RM, Moran JJ, Mazuski JE, et al. Multiple organ failure in trauma patients [J]. J Trauma, 2003, 55 (4): 608-616.
  • 6Spain DA, Fruchterman TM, Matheson PJ, et al. Complement activation mediates intestinal injury after resuscitation from hemorrhagic shock [J]. J Trauma, 1999, 46 (2): 224-233.
  • 7Magnotti LJ, Deitch EA. Bums, bacterial translocation, gut barrier function, and failure [J]. J Bum Care Rehabil, 2005, 26 (5): 383- 391.
  • 8Keel M, Trentz O. Pathophysiology of polytrauma [J]. Injury, 2005, 36 (6) : 691-709.
  • 9Hart ML, Walsh MC, Stahl GL. Intitiation of complement activation following oxidative stress. In vitro and in vivo observations [J]. Mol Immuno, 2004, 41 (2): 165-171.
  • 10Fosbrink M, Niculescu F, Rus H. The role of c5b-9 terminal complement complex in activation of the cell cycle and transcription [J]. Immunol Res, 2005, 31 (1): 37-46.

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