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半胱胺诱发大鼠十二指肠溃疡及胃酸分泌

Cysteamine-induced duodenal ulcer and acid secretion in the rat.

作者信息

Kirkegaard P, Poulsen S S, Loud F B, Halse C, Christiansen J

出版信息

Scand J Gastroenterol. 1980;15(5):621-4. doi: 10.3109/00365528009182225.

Abstract

Duodenal ulcers can be produced in rats within 24 h by a single subcutaneous administration of cysteamine. To determine the role of gastric acid secretion in the pathogenesis of these ulcers, secretory and pathoanatomic studies were performed in chronic fistula rats ater an ulcerogenic dose of cysteamine. A prolonged increase of acid secretion was seen after cysteamine, reaching fourfold the basal level after 5 h. The acid response lasted for 10 to 11 h. After vagotomy cysteamine-induced acid secretion was markedly reduced. Ulcer formation was prevented by vagotomy and by drainage of the gastric juice before it entered the duodenum. When a gastric acid output equivalent to that produced by the ulcerogenic dose of cysteamine was induced by repeated injections of pentagastrin, no mucosal changes were seen in the duodenum. These results indicate that, although some acid in the duodenum is required for ulcer formation, the hypersecretion of acid induced by cysteamine is not the only factor responsible for the development of duodenal ulcer.

摘要

通过单次皮下注射半胱胺,可在24小时内使大鼠产生十二指肠溃疡。为确定胃酸分泌在这些溃疡发病机制中的作用,在给予致溃疡剂量的半胱胺后,对慢性瘘管大鼠进行了分泌和病理解剖学研究。半胱胺注射后可见胃酸分泌持续增加,5小时后达到基础水平的四倍。酸反应持续10至11小时。迷走神经切断术后,半胱胺诱导的胃酸分泌明显减少。迷走神经切断术以及在胃液进入十二指肠之前将其引流可预防溃疡形成。当通过反复注射五肽胃泌素诱导出与致溃疡剂量的半胱胺所产生的胃酸分泌量相当的胃酸分泌时,十二指肠未出现黏膜变化。这些结果表明,虽然十二指肠溃疡形成需要一定量的胃酸,但半胱胺诱导的胃酸分泌过多并非十二指肠溃疡发生的唯一因素。

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