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[组胺诱导离体犬肠系膜动脉和静脉舒张的机制]

[Mechanisms of histamine-induced relaxation in isolated dog mesenteric arteries and veins].

作者信息

Yamazaki M, Toda N

机构信息

Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.

出版信息

Nihon Yakurigaku Zasshi. 1992 Jan;99(1):19-26. doi: 10.1254/fpj.99.19.

Abstract

Mechanisms of histamine-induced relaxation in dog mesenteric artery and vein strips were compared. Histamine elicited a concentration-related relaxation in the arterial strips contracted with prostaglandin (PG) F2 alpha; the relaxations induced at 5 x 10(-7) M or higher were composed of phasic and tonic patterns. The phasic component of relaxation was inhibited by chlorpheniramine, but not by cimetidine. Combined treatment with the H1 and H2 antagonists abolished the amine-induced relaxation. The tonic component was inhibited by cimetidine. The phasic relaxation was attenuated by removal of the endothelium. Treatment with indomethacin inhibited the phasic component in the strips with endothelium, but did not influence the relaxation after endothelium denudation. Combined treatment with indomethacin and cimetidine, but not chlorpheniramine, abolished the response. On the other hand, histamine produced a concentration-related, tonic relaxation in the mesenteric vein strips. The relaxation was not influenced by indomethacin, endothelium-denudation, and chlorpheniramine, but was abolished by cimetidine. It may be concluded that the phasic relaxation of dog mesenteric arterial strips is mediated mainly by H1 receptors in the endothelium, resulting in the synthesis and release of PGI2. The tonic relaxation appears to be elicited by activation of H2 receptors in smooth muscle. Mesenteric vein relaxations induced by histamine are likely to be mediated solely by H2 receptors in smooth muscle.

摘要

比较了组胺诱导犬肠系膜动脉和静脉条带舒张的机制。组胺使用前列腺素(PG)F2α收缩的动脉条带产生浓度依赖性舒张;在5×10⁻⁷M或更高浓度诱导的舒张由相性和持续性模式组成。相性舒张成分被氯苯那敏抑制,但不被西咪替丁抑制。H1和H2拮抗剂联合处理可消除胺诱导的舒张。持续性成分被西咪替丁抑制。去除内皮后相性舒张减弱。吲哚美辛处理抑制了有内皮条带中的相性成分,但不影响内皮剥脱后的舒张。吲哚美辛和西咪替丁联合处理(而非氯苯那敏)可消除反应。另一方面,组胺在肠系膜静脉条带中产生浓度依赖性的持续性舒张。该舒张不受吲哚美辛、内皮剥脱和氯苯那敏的影响,但被西咪替丁消除。可以得出结论,犬肠系膜动脉条带的相性舒张主要由内皮中的H1受体介导,导致前列环素(PGI2)的合成和释放。持续性舒张似乎是由平滑肌中H2受体的激活引起的。组胺诱导的肠系膜静脉舒张可能仅由平滑肌中的H2受体介导。

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