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下丘脑与胃黏膜损伤:应激性损伤的根源?

The hypothalamus and gastric mucosal injuries: origin of stress-induced injury?

作者信息

Salim A S

机构信息

Department of Surgery, Royal Infirmary, Perth, U.K.

出版信息

J Psychiatr Res. 1988;22(1):35-42. doi: 10.1016/0022-3956(88)90026-x.

Abstract

This paper reviews the role of the central nervous system in the genesis of gastrointestinal mucosal injuries. The discussion makes particular reference to the significance and mechanism of stress-induced injury of the gastroduodenal mucosa. It points out that in the rat, stress activates the hypothalamus, producing delivery of alpha-adrenergic stimulation to the stomach by the adrenergic hypothalamovagal pathway. This stimulation controls intragastric blood flow and 5-HT release. Low magnitude pharmacologically-induced stress enhances gastric acid secretion and, if this stress is maintained, it produces chronic duodenal ulceration. High magnitude pharmacologically-induced stress depresses acid secretion and injures the gastric mucosa. If such stress is maintained, it produces chronic gastric ulceration. The paper provides a detailed account of the mechanisms of these stress-induced gastroduodenal effects.

摘要

本文综述了中枢神经系统在胃肠道黏膜损伤发生过程中的作用。讨论特别提及了应激诱导的胃十二指肠黏膜损伤的意义和机制。指出在大鼠中,应激激活下丘脑,通过肾上腺素能下丘脑迷走神经通路向胃传递α-肾上腺素能刺激。这种刺激控制胃内血流和5-羟色胺释放。低强度药物诱导的应激增强胃酸分泌,如果这种应激持续存在,会导致慢性十二指肠溃疡。高强度药物诱导的应激抑制胃酸分泌并损伤胃黏膜。如果这种应激持续存在,会导致慢性胃溃疡。本文详细阐述了这些应激诱导的胃十二指肠效应的机制。

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