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应激及自主神经阻滞剂对大鼠胃黏膜微循环的影响。

Effects of stress and of autonomic blockers on gastric mucosal microcirculation in rats.

作者信息

Dai S, Ogle C W

出版信息

Eur J Pharmacol. 1975 Jan;30(1):86-92. doi: 10.1016/0014-2999(75)90207-1.

Abstract

Changes in gastric mucosal microcirculation in rats were studied by using the method of intra-aortic injection of India ink, followed by microdissection of the mucosa. Acute stress, induced by restraint and exposure to cold for 2 hr, caused marked and significant vasodilatation in the gastric mucosa. This vasodilatation was prevented by pretreatment with atropine or chlorpromazine, but not by alpha- or theta-adrenoceptor blocking agents. Phentolamine caused significant vasoconstriction in the gastric mucosa of non-stressed rats, but when animals were stressed phentolamine induced a greater vasodilatation than was obtained with stress alone. These observations provide added support for the hypothesis that stress induces vagal overactivity, probably of central origin. The resulting strong contractions of the gastric wall, and compression of the intramural vessels, are probably responsible for degeneration of the mucosal cells leading to the formation of stress-induced ulcers in the rat.

摘要

采用主动脉内注射印度墨水,随后对黏膜进行显微解剖的方法,研究大鼠胃黏膜微循环的变化。通过束缚和暴露于寒冷环境2小时诱导的急性应激,可导致胃黏膜明显且显著的血管扩张。预先用阿托品或氯丙嗪处理可预防这种血管扩张,但α或θ肾上腺素能受体阻断剂则不能。酚妥拉明可使未受应激大鼠的胃黏膜产生显著的血管收缩,但当动物受到应激时,酚妥拉明诱导的血管扩张比单独应激时更大。这些观察结果为应激诱导迷走神经活动过度(可能源于中枢)这一假说提供了更多支持。胃壁由此产生的强烈收缩以及对壁内血管的压迫,可能是导致大鼠黏膜细胞变性并形成应激性溃疡的原因。

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