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[生物胺受体阻断剂对实验性溃疡形成的影响]

[Effect of blockaders of biogenic amine receptors on experimental ulcer development].

作者信息

Karevina T G, Shevchuk I M

出版信息

Farmakol Toksikol. 1988 Jul-Aug;51(4):56-60.

PMID:2847940
Abstract

The effects of serotonin antagonist peritol, cholinolytic atropine, H2-receptor blocker cimetidine and dopaminergic receptor blocker metoclopramide on stress- and exogenous serotonin-induced gastric ulcerogenesis in rats were studied. Peritol was shown to inhibit significantly serotonin- an stress-induced hemorrhagic effect. Similar but less pronounced inhibit produced by metoclopramide and cimetidine. Atropine decreased gastric hemorrhages induced by serotonin but failed to affect stress-induced hemorrhagic lesions. All antagonists tested decreased stress-induced erosions. Erosive lesions stimulated by exogenous serotonin were significantly decreased by atropine only. Metoclopramide known for its cholinomimetic action increased serotonin-induced erosions. It was concluded that serotonin plays an essential role in the pathogenesis of gastric lesions, and its effects suggest the involvement of acetylcholine, histamine and dopamine.

摘要

研究了5-羟色胺拮抗剂派利醇、抗胆碱药阿托品、H2受体阻滞剂西咪替丁和多巴胺能受体阻滞剂甲氧氯普胺对大鼠应激和外源性5-羟色胺诱导的胃溃疡形成的影响。结果表明,派利醇能显著抑制5-羟色胺和应激诱导的出血效应。甲氧氯普胺和西咪替丁也有类似作用,但效果较弱。阿托品可减少5-羟色胺诱导的胃出血,但对应激诱导的出血性损伤无效。所有测试的拮抗剂均能减少应激诱导的糜烂。仅阿托品能显著减少外源性5-羟色胺刺激引起的糜烂性损伤。以拟胆碱作用著称的甲氧氯普胺会增加5-羟色胺诱导的糜烂。结论是,5-羟色胺在胃损伤的发病机制中起重要作用,其作用表明乙酰胆碱、组胺和多巴胺也参与其中。

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