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体温过低引起的胃酸过多和胃黏膜损伤与大鼠脑内γ-氨基丁酸(GABA)浓度升高有关。

Gastric hyperacidity and mucosal damage caused by hypothermia correlate with increase in GABA concentrations of the rat brain.

作者信息

Hara N, Hara Y, Natsume Y, Goto Y

机构信息

Research Laboratories, Sumitomo Pharmaceuticals Co., Ltd., Osaka, Japan.

出版信息

Eur J Pharmacol. 1991 Feb 26;194(1):77-81. doi: 10.1016/0014-2999(91)90126-b.

Abstract

The involvement of brain GABA mechanisms in acid secretion and maintenance of gastric mucosal integrity was studied in the anesthetized rat. Cold exposure lowered the rectal temperature and stimulated acid output in the anesthetized rat. The acid response to cold exposure was completely suppressed by surgical vagotomy. The substantial increase in brain GABA content evoked by pretreatment with aminooxyacetic acid (10 and 20 mg/kg s.c. x 3) significantly potentiated the gastric acid response to the cold exposure stress; suppression of the GABA content induced by semicarbazide (100 mg/kg s.c.) reduced the acid response to cold. Significant correlations were found between the brain GABA contents and the acid secretory activity and also between the GABA contents and the ulcer index of gastric lesions induced by the cold stress. These results indicate that hypothermia evoked by cold exposure stimulates gastric acid secretion and induces gastric lesions through central GABA mechanisms in the rat.

摘要

在麻醉大鼠中研究了脑γ-氨基丁酸(GABA)机制在胃酸分泌和胃黏膜完整性维持中的作用。冷暴露降低了麻醉大鼠的直肠温度并刺激了胃酸分泌。冷暴露引起的酸反应被手术切断迷走神经完全抑制。用氨氧乙酸(10和20mg/kg皮下注射×3)预处理引起的脑GABA含量大幅增加显著增强了胃酸对冷暴露应激的反应;氨基脲(100mg/kg皮下注射)诱导的GABA含量抑制降低了对冷的酸反应。在脑GABA含量与酸分泌活性之间以及GABA含量与冷应激诱导的胃损伤溃疡指数之间发现了显著相关性。这些结果表明,冷暴露引起的体温过低通过大鼠中枢GABA机制刺激胃酸分泌并诱导胃损伤。

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