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左旋多巴在有无抑制脑外多巴脱羧酶情况下对人体胃酸分泌和胃泌素释放的影响。

Effect of L-dopa with and without inhibition of extra cerebral dopa decarboxylase on gastric acid secretion and gastrin release in man.

作者信息

Caldara R, Barbieri C, Piepoli V, Borzio M, Masci E

出版信息

Gut. 1985 Oct;26(10):1014-7. doi: 10.1136/gut.26.10.1014.

Abstract

The present study was undertaken to investigate the possibility that central nervous system monoaminergic pathways may play a role in the control of gastric acid and gastrin secretion in man. Submaximal pentagastrin stimulated (0.25 micrograms/kg/h) gastric acid secretion, as well as basal gastrin concentrations were studied in two groups of subjects. The first group received oral administration of placebo and the catecholamine precursor L-dopa (500 mg); the second group was treated with placebo and the association of L-dopa (100 mg) plus carbidopa (35 mg) after pretreatment with carbidopa (50 mg every six hours for four doses), a schedule which is known to increase brain catecholamine concentrations. In comparison with placebo, stimulated gastric acid secretion was reduced by L-dopa alone, whereas was not modified by L-dopa plus carbidopa. Basal gastrin concentrations were increased after L-dopa and after L-dopa plus carbidopa. These data show that basal gastrin concentration is raised by central catecholamine augmentation; but gastric acid secretion seems to be influenced by changes of peripheral catecholamine concentrations. It is suggested that dopamine and perhaps noradrenaline, but not adrenaline, are important in these effects.

摘要

本研究旨在探讨中枢神经系统单胺能通路可能在人类胃酸和胃泌素分泌控制中发挥作用的可能性。在两组受试者中研究了次最大剂量的五肽胃泌素刺激(0.25微克/千克/小时)胃酸分泌以及基础胃泌素浓度。第一组口服安慰剂和儿茶酚胺前体左旋多巴(500毫克);第二组在先用卡比多巴(每6小时50毫克,共4剂)预处理后,用安慰剂以及左旋多巴(100毫克)加卡比多巴(35毫克)联合治疗,该方案已知可增加脑内儿茶酚胺浓度。与安慰剂相比,单独使用左旋多巴可降低刺激后的胃酸分泌,而左旋多巴加卡比多巴则无此作用。左旋多巴及左旋多巴加卡比多巴治疗后基础胃泌素浓度均升高。这些数据表明,中枢儿茶酚胺增加可提高基础胃泌素浓度;但胃酸分泌似乎受外周儿茶酚胺浓度变化的影响。提示多巴胺以及可能去甲肾上腺素而非肾上腺素在这些作用中起重要作用。

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本文引用的文献

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Decrease of cerebral 5-hydroxytryptamine by 3,4-dihydroxyphenylalanine after inhibition of extracerebral decarboxylase.
J Pharm Pharmacol. 1968 Mar;20(3):228-9. doi: 10.1111/j.2042-7158.1968.tb09726.x.

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