Tariq M
Toxicol Lett. 1987 Jun;37(1):63-8. doi: 10.1016/0378-4274(87)90168-8.
The effect of endotoxin pretreatment (1 mg/kg body weight, i.p., once daily for 2 days) on the gastric mucosal damage induced by aspirin, phenylbutazone and reserpine has been studied in albino rats. When given alone, endotoxin did not produce any visibly discernible gastric lesions. It produced a significant augmentation of the gastric lesions produced by phenylbutazone and reserpine but did not significantly alter the ulcerogenicity of aspirin. The involvement of endogenous histamine formation and its release following phenylbutazone and reserpine administration and also in response to endotoxin pretreatment may be responsible for the exacerbation of gastric lesions induced by these drugs. Recent reports indicate the involvement of endorphins and platelet activating factor (PAF) in the ulcerogenic activity of endotoxin when used in high doses and their role in the potentiation of phenylbutazone- and reserpine-induced gastric lesions has to be worked out.
在内毒素预处理（1毫克/千克体重，腹腔注射，每日一次，共2天）对白化大鼠由阿司匹林、保泰松和利血平诱导的胃黏膜损伤的影响方面进行了研究。单独给予内毒素时，不会产生任何明显可见的胃部病变。它显著增强了保泰松和利血平所产生的胃部病变，但并未显著改变阿司匹林的致溃疡作用。内源性组胺形成及其在保泰松和利血平给药后以及对内毒素预处理的反应中的释放，可能是这些药物诱导的胃部病变加剧的原因。最近的报告表明，高剂量使用内毒素时，内啡肽和血小板活化因子（PAF）参与其致溃疡活性，它们在增强保泰松和利血平诱导的胃部病变中的作用有待研究。
