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可乐定对乙醇诱导的胃损伤的加重作用:可能的作用机制。

Aggravating action of clonidine on ethanol-induced gastric lesions: probable mechanism of action.

作者信息

D'Souza R S, Bhandare P N, Dhume V G

机构信息

Department of Pharmacology, Goa Medical College, Bambolim, St. Cruz.

出版信息

Indian J Physiol Pharmacol. 1990 Oct;34(4):252-4.

PMID:1966047
Abstract

Large doses of the imidazoline alpha 2 adrenoreceptor agonist clonidine aggravate ethanol-induced gastric lesions. The alpha 2 adrenoceptor antagonist phentolamine, the opioid antagonist naloxone and the H2 antagonist cimetidine do not prevent this action of clonidine suggesting that it is not mediated by alpha 2, opioid or H2 receptors. Further, like clonidine, high doses of phentolamine and cimetidine aggravate gastric lesions per se, suggesting that all three may be acting at a common 'receptor' site, possibly the imidazoline-preferring receptor (IPR).

摘要

大剂量的咪唑啉α2肾上腺素能受体激动剂可乐定可加重乙醇诱导的胃部损伤。α2肾上腺素能受体拮抗剂酚妥拉明、阿片受体拮抗剂纳洛酮和H2拮抗剂西咪替丁均不能阻止可乐定的这一作用,这表明其并非由α2、阿片或H2受体介导。此外,与可乐定一样,高剂量的酚妥拉明和西咪替丁本身也会加重胃部损伤,这表明这三种药物可能作用于一个共同的“受体”位点,可能是咪唑啉优先受体(IPR)。

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