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乙醇和尼古丁对大鼠胃泌素和生长抑素释放的影响。

Effects of ethanol and nicotine on gastrin and somatostatin release in rats.

作者信息

Cho C H, Ogle C W, Wong S H, Lam S K

出版信息

Horm Res. 1987;25(2):113-9. doi: 10.1159/000180641.

Abstract

An intravenous bolus injection of nicotine (1 mg/kg) markedly elevated gastric acid secretion; oral administration of ethanol (40%, 10 ml/kg) significantly increased arterial serum gastrin and somatostatin levels. Chronic pretreatment with oral nicotine (5 or 25 micrograms/ml in drinking tap water, for 10 days), but not acute pretreatment with a single oral dose of nicotine (2 or 4 mg/kg), inhibited the nicotine-induced gastric acid secretion and ethanol-induced gastrin and somatostatin release. Pretreatment subcutaneously with a ganglion-blocking dose of hexamethonium (10 mg/kg), however, inhibited nicotine-stimulated acid output and ethanol-evoked somatostatin secretion but not ethanol-induced gastrin release. It is concluded that ethanol-evoked gastrin secretion could be due to activation of specific sites which are not nicotinic receptors, but which are depressed by chronic nicotine pretreatment. On the other hand, the release of somatostatin by ethanol appears to be controlled by ganglionic receptors in the gut.

摘要

静脉推注尼古丁(1毫克/千克)可显著提高胃酸分泌;口服乙醇(40%,10毫升/千克)可显著提高动脉血清胃泌素和生长抑素水平。用口服尼古丁(自来水中5或25微克/毫升,持续10天)进行慢性预处理,但单次口服尼古丁(2或4毫克/千克)进行急性预处理则不会,可抑制尼古丁诱导的胃酸分泌以及乙醇诱导的胃泌素和生长抑素释放。然而,用神经节阻断剂量的六甲铵(10毫克/千克)进行皮下预处理,可抑制尼古丁刺激的酸分泌以及乙醇诱发的生长抑素分泌,但不能抑制乙醇诱导的胃泌素释放。得出的结论是,乙醇诱发的胃泌素分泌可能是由于特定部位的激活,这些部位不是烟碱受体,但会被慢性尼古丁预处理所抑制。另一方面,乙醇诱导的生长抑素释放似乎受肠道神经节受体控制。

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