白三烯D4在感染性休克模型中的作用。

Eicosanoids Pub Date : 1992-01-01
T Hartung, G Tiegs, A Wendel
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引用次数: 0

摘要

感染性休克是重症监护患者治疗过程中的主要并发症。在啮齿类动物实验中,内毒素也可引起类似的病理状态。有间接和直接的证据表明白三烯D4参与了这个实验性的多器官衰竭。由于半乳糖胺内毒素引起的肝脏特异性敏感,实验上可以将多器官衰竭转移到单个器官,即肝衰竭。本文提供的数据显示,二十烷类白三烯D4在两种脓毒症模型中都有参与。我们最近描述了一个模拟内毒素引起的肝衰竭的细胞系统。在这个以肝细胞和非实质肝细胞共培养为基础的系统中,白三烯D4是细胞毒性发展所必需的。结论是,这三种模型共享关键的机制原理,可以相互补充,以研究潜在的分子事件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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The role of leukotriene D4 in septic shock models.

Septic shock is a major complication during the treatment of intense care patients. A similar pathologic state can be experimentally induced in rodents by application of endotoxins. There is circumstantial as well as direct evidence for a participation of leukotriene D4 in this experimental multiorgan failure. Due to liver-specific sensitivation by galactosamine endotoxin-induced multiorgan failure can be experimentally transposed to a single organ, i.e. hepatic failure. Data presented here show a participation of the eicosanoid leukotriene D4 in either model of sepsis. We have recently described a cellular system modelling endotoxin-induced hepatic failure. In this system based on the coculture of hepatocytes and nonparenchymal liver cells leukotriene D4 is required for the development of cytotoxicity. It is concluded that the three models share pivotal mechanistic principles and might be used complementary to each other in order to study underlying molecular events.

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