Osumi Y, Ishikawa T, Nagasaka Y, Fujiwara M
Eur J Pharmacol. 1980 Dec 19;68(4):409-15. doi: 10.1016/0014-2999(80)90415-x.
The central effect of nicotine on gastric acid secretion was examined in rats anesthetized with urethane. Intraventricular administration of nicotine 5 and 20 microgram/animal induced a dose-related increase in acid output. This nicotine-induced increase was blocked by treatment with hexamethonium 50 microgram/animal given intraventricularly or atropine 100 microgram/kg given intravenously. Changes in acid output after intravenous administration of nicotine 100 microgram/kg were inconsistent; however, a significant increase was observed with 500 microgram/kg of this alkaloid given by the same route. This increase was also blocked by hexamethonium 50 microgram/animal given intraventricularly. The level of gastrin in the gastric juice, after the intraventricular administration of nicotine 20 microgram/animal, did not significantly differ from the control. These results suggest that nicotine administered intraventricularly stimulates nicotinic receptors in the brain, and that there is a subsequent excitation of cholinergic muscarinic receptors in the stomach after which the secretion of acid increases.
在用乌拉坦麻醉的大鼠中研究了尼古丁对胃酸分泌的中枢作用。脑室内给予尼古丁5和20微克/只动物,可引起胃酸分泌量呈剂量相关增加。脑室内给予六甲铵50微克/只动物或静脉注射阿托品100微克/千克可阻断尼古丁引起的这种增加。静脉注射尼古丁100微克/千克后胃酸分泌量的变化不一致;然而,通过相同途径给予500微克/千克这种生物碱时,观察到显著增加。脑室内给予六甲铵50微克/只动物也可阻断这种增加。脑室内给予尼古丁20微克/只动物后,胃液中胃泌素水平与对照组无显著差异。这些结果表明,脑室内给予尼古丁可刺激脑中的烟碱受体,随后胃中的胆碱能毒蕈碱受体兴奋,进而胃酸分泌增加。