PREVENTION OF ETHANOL AND ASPIRIN-INDUCED GASTRIC-MUCOSAL LESIONS BY PARACETAMOL AND SALICYLATE IN RATS - ROLE OF ENDOGENOUS PROSTAGLANDINS
PREVENTION OF ETHANOL AND ASPIRIN-INDUCED GASTRIC-MUCOSAL LESIONS BY PARACETAMOL AND SALICYLATE IN RATS - ROLE OF ENDOGENOUS PROSTAGLANDINS
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DOI：
10.1136/gut.23.6.536
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发表时间：
1982-01-01
期刊：
影响因子：
24.5
通讯作者：
RADECKI, T
中科院分区：
文献类型：
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作者：
KONTUREK, SJ;BRZOZOWSKI, T;RADECKI, T
在给予无水乙醇或酸化阿司匹林前30分钟灌胃给予对乙酰氨基酚或水杨酸钠，可剂量依赖性地减少粘膜病变的形成。产生的胃粘膜类胰头素活性增加与乙醇和酸化阿司匹林完全抑制。对乙酰氨基酚或水杨酸钠单独给药可增加粘膜中类胰高血糖素物质的生成。前列腺素合成抑制剂吲哚美辛抑制了这种作用，并抑制了对乙酰氨基酚或水杨酸钠对胃损伤产生的保护作用。
Paracetamol or sodium salicylate given intragastrically 30 min before the administration of absolute ethanol or acidified aspirin dose-dependently reduced the formation of mucosal lesions. The generation of gastric mucosal prostaglandin-like activity increased with ethanol and was completely suppressed by acidified aspirin. Paracetamol or sodium salicylate given alone increased the generation of mucosal prostaglandin-like material. Indomethacin, the prostaglandin synthesis inhibitor, suppressed this effect and inhibited the protective influence of paracetamol or sodium salicylate on the production of gastric lesions.