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阿托品未能抑制人胃泌素-17对食管下括约肌的刺激作用。

Failure of atropine to inhibit gastrin-17 stimulation of the lower esophageal sphincter in man.

作者信息

Jensen D M, McCallum R, Walsh J H

出版信息

Gastroenterology. 1978 Nov;75(5):825-7.

PMID:359401
Abstract

Heptadecapeptide gastrin I (G-17) contrast the lower esophageal sphincter (LES) in man and animals. Previous studies in man found that atropine infusion (12 microgram kg-1hr-1) inhibited the effect of gastrin on the LES, suggesting that this effect of gastrin is mediated by a cholinergic mechanism. Studies in the opossum have not shown similar inhibition. To reevaluate the interaction of atropine and G-17 on the LES, 5 normal males were studied. Submaximal and maximal effective doses of G-17 were used with both atropine infusion (12 microgram kg-1hr-1) and rapid intravenous injection (1 mg). There was a small decrease in basal LES pressure with atropine infusion. However, neither atropine infusion nor rapid intravenous injection inhibited LES stimulation by submaximal and maximal doses of G-17. The results do not support the hypothesis that LES responses to gastrin are mediated by an atropine-sensitive cholinergic mechanism.

摘要

十七肽胃泌素I(G - 17)可使人和动物的食管下括约肌(LES)收缩。以往对人体的研究发现,输注阿托品(12微克/千克·小时)可抑制胃泌素对LES的作用,提示胃泌素的这种作用是通过胆碱能机制介导的。对负鼠的研究未显示出类似的抑制作用。为了重新评估阿托品与G - 17对LES的相互作用,对5名正常男性进行了研究。使用亚最大和最大有效剂量的G - 17,同时进行阿托品输注(12微克/千克·小时)和快速静脉注射(1毫克)。输注阿托品时,基础LES压力略有下降。然而,无论是阿托品输注还是快速静脉注射,均未抑制亚最大和最大剂量G - 17对LES的刺激作用。这些结果不支持LES对胃泌素的反应是由对阿托品敏感的胆碱能机制介导的这一假说。

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