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胃十二指肠黏膜损伤的途径、介质和机制。

Pathways, mediators and mechanisms of gastroduodenal mucosal injury.

作者信息

Szabo S, Nagy L

机构信息

Department of Pathology, Brigham & Women's Hospital, Boston, MA 02115.

出版信息

Acta Physiol Hung. 1992;80(1-4):9-21.

PMID:1345211
Abstract

This review provides evidence that gastroduodenal mucosal injury is a complex process because of the heterogeneous structure and multiple functions of the gut. The action of exogenous etiologic agents is usually mediated in part, or amplified by endogenous mediators which very often exert biphasic, i.e., damaging and protective effects. The pathogenetic pathways involve direct/indirect chemical injury, vascular damage and its consequences, and acute or chronic inflammatory processes following infectious, chemical or ischemic injury. The role of oxygen, free radicals, calcium and proteases as well as the components and forms of gastroduodenal injury, e.g., reversible and irreversible cell injury, tissue necrosis, acute and chronic inflammation are also briefly discussed. Only a slight or moderate direct cytoprotection was demonstrated in vitro using isolated, mixed rat gastric mucosal cells by the known gastroprotective drugs including PG and SH compounds. Thus, the terms of organo or gastroprotection are more descriptive then the misleading "gastric cytoprotection".

摘要

本综述提供的证据表明,由于肠道结构的异质性和多种功能,胃十二指肠黏膜损伤是一个复杂的过程。外源性病因的作用通常部分由内源性介质介导,或被其放大,而内源性介质常常产生双相作用,即损伤和保护作用。发病机制涉及直接/间接化学损伤、血管损伤及其后果,以及感染性、化学性或缺血性损伤后的急性或慢性炎症过程。还简要讨论了氧、自由基、钙和蛋白酶的作用,以及胃十二指肠损伤的组成和形式,如可逆和不可逆细胞损伤、组织坏死、急性和慢性炎症。使用包括PG和SH化合物在内的已知胃保护药物,在体外对分离的混合大鼠胃黏膜细胞进行实验,仅证明了轻微或中度的直接细胞保护作用。因此,“器官保护”或“胃保护”术语比具有误导性的“胃细胞保护”更具描述性。

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