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十二指肠溃疡的发病机制。大鼠中丙腈和半胱胺引起的胃酸过多。

Pathogenesis of duodenal ulcer. Gastric hyperacidity caused by propionitrile and cysteamine in rats.

作者信息

Szabo S, Reynolds E S, Lictenberger L M, Haith L R, Dzau V J

出版信息

Res Commun Chem Pathol Pharmacol. 1977 Feb;16(2):311-23.

PMID:847287
Abstract

Cysteamine and propionitrile, experimental duodenal ulcerogens, stimulated gastric acid secretion in the rat. Gastric acid secretion was measured by two separate methods, the conventional pylorus ligation technique and a non-invasive technique based on the pH dependent liberation of azure A from azuresin in the stomach with subsequent excretion of the liberated dye in the urine. Volume, acid concentration and acid content of gastric fluids aspirated immediately before the pylrous ligation were markedly increased 1,4 and 7 hours after a single dose of either cysteamine or propionitrile. Both acid concentration and acid output of gastric contents collected 30 minutes after pylorus ligation were also significantly elevated 1.5 hours after propionitrile and 4.5 hours after cysteamine. Significant increases in gastric acid secretion after these chemicals were also measured by the non-invasive technique which demonstrated a 4 to 6 fold increase in 24 hour urinary azure A output in rats injected with either propionitrile or cysteamine. Enhanced gastric acid output may play an important role in the pathogenesis of duodenal ulcer produced by propionitrile and cysteamine.

摘要

半胱胺和丙腈是实验性十二指肠溃疡诱发剂,可刺激大鼠胃酸分泌。胃酸分泌通过两种不同方法进行测量,即传统的幽门结扎技术和一种基于胃中天青A从天青树脂依pH值释放并随后在尿液中排泄游离染料的非侵入性技术。在单次给予半胱胺或丙腈后1、4和7小时,紧接幽门结扎前抽取的胃液体积、酸浓度和酸含量显著增加。幽门结扎30分钟后收集的胃内容物的酸浓度和酸排出量在丙腈给药后1.5小时和半胱胺给药后4.5小时也显著升高。这些化学物质给药后胃酸分泌的显著增加也通过非侵入性技术测得,该技术表明注射丙腈或半胱胺的大鼠24小时尿中天青A排出量增加4至6倍。胃酸分泌增强可能在丙腈和半胱胺所致十二指肠溃疡的发病机制中起重要作用。

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Pathogenesis of duodenal ulcer. Gastric hyperacidity caused by propionitrile and cysteamine in rats.十二指肠溃疡的发病机制。大鼠中丙腈和半胱胺引起的胃酸过多。
Res Commun Chem Pathol Pharmacol. 1977 Feb;16(2):311-23.
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