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Study on the mechanical analysis of septic shock and its theraputic strategy

感染性休克的力学分析及治疗策略研究

基本信息

批准号：
62480271
负责人：
KODAMA Masashi
金额：
$ 4.42万
依托单位：
Shiga University of Medical Science School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

Analysis of shock mecanism. We re-evaluate the TNF/Cachectin which plays a main role in septic shock. We re-examine the shock-action of recombinant TNF (Dai Nippon Phamaco.). This method has been re-employed in the same model by Cerami. This kind of TNF does not induce the shock state in the rat. This TNF containd much less endotoxin ( 20 pg-LPS/g-TNF ) than TNF (0.4mu/mg-TNF) used by Cerami. But our TNF plus LPS administration could lead the rat into the shock state. According to this results, small amount of LPS and TNF act more stronger than each one. Simillary we re-studied leukotoxin (reported by Ozawa) which is one of the shock-inducing madiator. Synthetic leucotoxin was injected into rat. They died in a result of severe lung hemorrhage without hypotension. Their death is concidered to be caused by shwartzman reaction. These results indicate that TNF or Leukotoxin does not play a main substance leading to septic shock. We are now performing further study on IL-1. Treatment of septic shock in the dog by PMX-F or protease inhibitor (Urinastatin). We performed the PMX-F treatment for the E. coli-induced septic shock. PMX-F treatment prolonged the survival time (Control group; 18 hr<,Treated group; 3-7 days>). Various parameters (mainly bacterial counts, serum-glucose level) improving in the PMX-F treatment group. We performed the same above mentioned experiment by using urinastatin instead of PMX-F. By this treatment, canine was prolonged survival time and improved cardiac output, hypotension, RES-function itself.

冲击机理分析。我们重新评估在败血性休克中起主要作用的 TNF/Cachectin。我们重新检验重组TNF（Dai Nippon Phamaco.）的休克作用。 Cerami 在同一模型中重新采用了该方法。这种TNF不会引起大鼠休克状态。该 TNF 含有的内毒素 (20 pg-LPS/g-TNF) 比 Cerami 使用的 TNF (0.4mu/mg-TNF) 少得多。但我们的 TNF 加 LPS 给药可能会导致大鼠进入休克状态。根据该结果，少量的LPS和TNF的作用比各自更强。同样，我们重新研究了白细胞毒素（小泽报道），它是一种引起休克的介质。将合成的白细胞毒素注射到大鼠体内。他们因严重肺出血而死亡，但没有出现低血压。他们的死亡被认为是由施瓦兹曼反应引起的。这些结果表明TNF或白细胞毒素并不是导致感染性休克的主要物质。我们现在正在对IL-1进行进一步的研究。用 PMX-F 或蛋白酶抑制剂（Urinastatin）治疗狗的感染性休克。我们对大肠杆菌引起的感染性休克进行了 PMX-F 治疗。 PMX-F治疗延长了生存时间（对照组；18小时<，治疗组；3-7天>）。 PMX-F 治疗组的各种参数（主要是细菌计数、血清血糖水平）有所改善。我们使用尿司他丁代替 PMX-F 进行了与上述相同的实验。通过这种治疗，犬的生存时间得到延长，心输出量、低血压、RES 功能本身得到改善。