ENDOTOXIN-INDUCED ORGAN INJURY

被引:94
作者
GHOSH, S
LATIMER, RD
GRAY, BM
HARWOOD, RJ
ODURO, A
机构
关键词
ENDOTOXIN; ORGAN FAILURE; MULTIPLE; LEUKOCYTES; TUMOR NECROSIS FACTOR-ALPHA; LEUKOTRIENES; COMPLEMENT; PROSTAGLANDINS; SPECIES SPECIFICITY; SHOCK; SEPTIC; CRITICAL ILLNESS;
D O I
10.1097/00003246-199302001-00005
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objective: To review the effects of endotoxemia on the major organ systems of the body and discuss potential mechanisms of tissue injury. Design: Appraisal of 60 articles representing a cross section of studies relating to in vivo and in vitro responses to endotoxin. Main Methods: Cell cultures, isolated tissue preparations, animal and human studies. Results: Endotoxemia results in the activation of numerous cellular and hematogenous mediators. These mediators range from prostaglandins, thromboxanes, and leukotrienes, to complement components. Tumor necrosis factor may be responsible for initiating many of the observed responses to endotoxin. Species and tissue specificity are a prominent feature of the response to endotoxin. Conclusions: No single agent can yet be implicated as the common mediator of endotoxin-induced organ injury. Endotoxin initiates the elaboration of a cascade of secondary mediators that amplify the response to the initial insult. The relative importance of individual agents as mediators of the response to endotoxin varies with the experimental model studied.
引用
收藏
页码:S19 / S24
页数:6
相关论文
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