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一氧化氮合酶抑制对禁食犬血浆胃动素释放的影响。

Effect of nitric oxide synthase inhibition on plasma motilin release in fasted dogs.

作者信息

Mizumoto A, Muramatsu S, Yamada T, Itoh Z

机构信息

Gastrointestinal Research Labs., Gunma University, Maebashi, Japan.

出版信息

Regul Pept. 1997 Jul 23;71(1):9-14. doi: 10.1016/s0167-0115(97)01004-5.

DOI:10.1016/s0167-0115(97)01004-5
PMID:9299636
Abstract

Inhibition of nitric oxide (NO) synthase on plasma motilin concentrations is not known. The aim of this study was to examine the effect of NO synthesis inhibitor on gastrointestinal motility and motilin release in conscious dogs. Dogs fitted with force transducers were given N omega-nitro-L-arginine (L-NNA) after the termination of phase III contractions. Blood samples were taken for measurement of motilin concentrations. L-NNA induced phase III-like contractions in the stomach in the duodenum in association with a significant increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Ondansetron markedly inhibited gastric, but not duodenal, phase III-like contractions without affecting the increase in motilin level caused by L-NNA. Vagotomy affected neither the occurence of phase III-like contractions nor the increase in motilin level produced by L-NNA. We conclude that inhibition of NO synthesis stimulates motilin release via cholinergic pathways independent of the vagus, and induces phase III-like contractions in the stomach and duodenum. Phase III-like contractions induced by L-NNA are mediated through the activation of 5-HT, receptors.

摘要

一氧化氮(NO)合酶对血浆胃动素浓度的抑制作用尚不清楚。本研究的目的是检测NO合成抑制剂对清醒犬胃肠动力和胃动素释放的影响。在III期收缩终止后,给安装有力传感器的犬静脉注射Nω-硝基-L-精氨酸(L-NNA)。采集血样以测定胃动素浓度。L-NNA可诱导胃和十二指肠出现类似III期的收缩,并伴有胃动素水平显著升高。阿托品或六甲铵可显著抑制L-NNA诱导的类似III期收缩及胃动素水平升高。昂丹司琼显著抑制胃而非十二指肠的类似III期收缩,但不影响L-NNA引起的胃动素水平升高。迷走神经切断术既不影响类似III期收缩的发生,也不影响L-NNA引起的胃动素水平升高。我们得出结论,抑制NO合成通过不依赖迷走神经的胆碱能途径刺激胃动素释放,并在胃和十二指肠诱导类似III期的收缩。L-NNA诱导的类似III期收缩是通过5-HT受体的激活介导的。

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