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多器官功能衰竭:炎症预激和激活序列促进自体组织损伤。

Multiple organ failure: inflammatory priming and activation sequences promote autologous tissue injury.

作者信息

Anderson B O, Harken A H

机构信息

University of Colorado Health Sciences Center, Denver 80262.

出版信息

J Trauma. 1990 Dec;30(12 Suppl):S44-9.

PMID:2174983
Abstract

Systemic inflammation promotes multiple organ failure through the induction of diffuse microvascular leak. Inflammatory cells such as neutrophils propagate this process. Tissue injury by neutrophils may be viewed as a normal process, inflammation, that has become uncontrolled and generalized. Multiple inflammatory stimuli synergistically promote neutrophil-mediated tissue injury in priming and activation sequences. In some settings, cellular priming is mediated by platelet-activating factor and can be prevented by platelet-activating factor antagonists. Inhibiting cellular priming could be efficacious in the therapy of multiple organ failure.

摘要

全身炎症通过诱导弥漫性微血管渗漏促进多器官功能衰竭。中性粒细胞等炎症细胞推动这一过程。中性粒细胞造成的组织损伤可被视为一种正常过程,即炎症,但其已变得不受控制并扩散开来。多种炎症刺激在启动和激活序列中协同促进中性粒细胞介导的组织损伤。在某些情况下,细胞启动由血小板活化因子介导,且可被血小板活化因子拮抗剂阻止。抑制细胞启动可能对多器官功能衰竭的治疗有效。

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Multiple organ failure: inflammatory priming and activation sequences promote autologous tissue injury.多器官功能衰竭:炎症预激和激活序列促进自体组织损伤。
J Trauma. 1990 Dec;30(12 Suppl):S44-9.
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Microvascular changes explain the "two-hit" theory of multiple organ failure.微血管变化解释了多器官功能衰竭的“两次打击”理论。
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Adaptive and maladaptive mechanisms of cellular priming.细胞致敏的适应性和适应不良机制。
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