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应激、肾上腺素能下丘脑 - 迷走神经通路与慢性十二指肠溃疡的病因学

Stress, the adrenergic hypothalamovagal pathway, and the aetiology of chronic duodenal ulceration.

作者信息

Salim A S

出版信息

J Psychosom Res. 1987;31(2):231-7. doi: 10.1016/0022-3999(87)90080-8.

Abstract

In the rat, stress activates the hypothalamus causing central adrenergic discharge with delivery of an alpha-adrenergic stimulus by the adrenergic hypothalamovagal pathway to the stomach. This stimulus controls intragastric blood flow and 5-HT release. In rats stressed pharmacologically by administration of intraperitoneal reserpine (0.1 mg/kg), the stimulated pathway releases gastric 5-HT which in turn significantly increases gastric acid secretion. Administration of intramuscular reserpine (0.1 mg/kg) every 24 hr for six weeks significantly (p less than 0.001 by Wilcoxon matched pairs signed-rank test) increased the basal acid output of the rat stomach (12 mumol/h +/- 0.5 vs 38.1 mumol/h +/- 2.4, mean +/- SEM) and produced duodenal ulceration in 83.3% of animals. Vagotomy completely protected the rat stomach against these effects. The data show that prolonged stress in the rat stimulates gastric acid secretion and produces duodenal ulceration.

摘要

在大鼠中,应激激活下丘脑,导致中枢肾上腺素能释放,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(5-HT)释放。在通过腹腔注射利血平(0.1mg/kg)进行药理学应激的大鼠中,受刺激的通路释放胃5-HT,进而显著增加胃酸分泌。每24小时肌肉注射利血平(0.1mg/kg),持续六周,显著(通过Wilcoxon配对符号秩检验,p<0.001)增加大鼠胃的基础酸分泌量(12μmol/h±0.5对38.1μmol/h±2.4,平均值±标准误),并在83.3%的动物中产生十二指肠溃疡。迷走神经切断术完全保护大鼠胃免受这些影响。数据表明,大鼠长期应激会刺激胃酸分泌并导致十二指肠溃疡。

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