可乐定的抗溃疡活性：对胃前列腺素无影响。

Antiulcer activity of clonidine: lack of effect on gastric prostaglandins.

作者信息

Ben-Zvi Z, Leibson V

机构信息

Clinical Pharmacology Unit, Faculty of Health Sciences, Ben Gurion University, Beer Sheva, Israel.

出版信息

Prostaglandins Leukot Med. 1987 Nov;30(1):51-9. doi: 10.1016/0262-1746(87)90024-2.

DOI:10.1016/0262-1746(87)90024-2

PMID:3481086

Abstract

Clonidine and paraaminoclonidine prevented the formation of indomethacin-induced gastric ulcers in female rats. This protective activity was blocked by coadministration of yohimbine. Therefore, the antiulcer activity of clonidine was due to its peripheral alpha-2 agonistic action. Because indomethacin is a prostaglandin synthetase inhibitor, its ulcerogenic effect has been attributed to a state of prostaglandin (PG) deficiency. We therefore investigated the possibility that the protective effect of alpha-2 adrenoceptor agonists could be mediated by stimulation of the biosynthesis of PGs in the stomach. However, the results failed to show increased production of PGE2 or 6-keto-PGF1, either in stomach slices in vitro or in the gastric mucosa of rats pretreated with clonidine, whether indomethacin was used or not. It is concluded that the activity of clonidine in preventing indomethacin-induced gastric erosions in rats is probably not related to prostaglandins.

摘要

可乐定和对氨基可乐定可预防吲哚美辛诱导的雌性大鼠胃溃疡形成。这种保护活性可被育亨宾共同给药所阻断。因此，可乐定的抗溃疡活性归因于其外周α-2激动作用。由于吲哚美辛是一种前列腺素合成酶抑制剂，其致溃疡作用被认为是由于前列腺素（PG）缺乏状态。因此，我们研究了α-2肾上腺素能受体激动剂的保护作用是否可通过刺激胃中PG的生物合成来介导。然而，无论是在体外胃切片中还是在经可乐定预处理的大鼠胃黏膜中，无论是否使用吲哚美辛，结果均未显示PGE2或6-酮-PGF1的产量增加。结论是，可乐定预防大鼠吲哚美辛诱导的胃糜烂的活性可能与前列腺素无关。