Hayden L J, Thomas G, West G B
J Pharm Pharmacol. 1978 Apr;30(4):244-6. doi: 10.1111/j.2042-7158.1978.tb13214.x.
The production by stress of gastric lesions in rats was inhibited by metiamide and by mepyramine. Lesions induced by indomethacin treatment were inhibited by mepyramine but not by metiamide. Those induced by aspirin treatment in pylorus-ligated rats were not affected by either antihistamine drug. Oral glutamine inhibited lesion production in all three systems whereas aspirin orally markedly potentiated it. Sodium salicylate inhibited both indomethacin-induced lesions and those produced by aspirin in pylorus-ligated rats. On the other hand, copper salicylate inhibited stress-induced lesions and it, like copper aspirinate, also markedly reduced the extent of lesions produced by aspirin. On the basis of these results, stress-induced lesion production offers a suitable animal model for testing anti-ulcer drugs as it is, like most human gastric ulcers, inhibited by H2-receptor inhibitors like metiamide.
甲硫米特和美吡拉敏可抑制应激引起的大鼠胃部损伤。美吡拉敏可抑制吲哚美辛治疗诱导的损伤,但甲硫米特不能。幽门结扎大鼠经阿司匹林治疗诱导的损伤,两种抗组胺药均无影响。口服谷氨酰胺可抑制所有三种模型中的损伤产生,而口服阿司匹林则明显增强损伤。水杨酸钠可抑制吲哚美辛诱导的损伤以及幽门结扎大鼠中阿司匹林产生的损伤。另一方面,水杨酸铜可抑制应激诱导的损伤,并且与阿司匹林铜一样,也显著降低阿司匹林产生的损伤程度。基于这些结果,应激诱导的损伤产生为测试抗溃疡药物提供了一个合适的动物模型,因为它与大多数人类胃溃疡一样,可被甲硫米特等H2受体抑制剂抑制。