The molecular pathogenesis of endotoxic shock and organ failure

被引：309

作者：

Karima, R ^{[1
]}

Matsumoto, S ^{[1
]}

Higashi, H ^{[1
]}

Matsushima, K ^{[1
]}

机构：

[1] Univ Tokyo, Fac Med, Bunkyo Ku, Dept Mol Prevent Med, Tokyo 113, Japan

来源：

MOLECULAR MEDICINE TODAY | 1999年 / 5卷 / 03期

关键词：

D O I：

10.1016/S1357-4310(98)01430-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Sepsis is still associated with a high mortality rate, Septic shock and sequential multiple organ failure have a strong correlation with poor outcome. Lipopolysaccharide (LPS) plays a pivotal role in the initiation of host responses to Gram-negative infection. A number of mediators, such as cytokines, nitric oxide and eicosanoids, are responsible far most of the manifestations caused by LPS, and circulatory failure, leukocyte-induced tissue injury and coagulation disorder appear to be critical determinants in the development of sequential organ failure. Although several anti-LPS or anti-cytokine clinical trials have been attempted, none of them has so far been successful.

引用

页码：123 / 132

页数：10

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