Nakamoto K, Kamisaki Y, Wada K, Kawasaki H, Itoh T
Department of Clinical Pharmacology, Faculty of Medicine, Tottori University, Yonago, Japan.
Pharmacology. 1997 Apr;54(4):203-10. doi: 10.1159/000139488.
We examined the effect of acetaminophen, an analgesic and antipyretic drug, on acute gastric mucosal injury induced by ischemia-reperfusion in rats. Ischemia-reperfusion was induced by clamping the celiac artery for 30 min with a small clip. Sixty minutes after reperfusion, the total area of erosions was measured. Acetaminophen (300 and 500 mg/kg) administered intraperitoneally 90 min before the ischemia significantly reduced the total area of erosions. The drug also inhibited the increase in lipid peroxide levels induced by ischemia-reperfusion in the gastric tissue and the increase in lipid peroxidation caused by the hydroxyl radical, OH., in vitro. Gastric prostaglandin E2 (PGE2) contents tended to increase after ischemia-reperfusion in both control and acetaminophen-treated groups. A significant difference in gastric PGE2 contents between control and acetaminophen-treated groups was not observed. The results indicate that acetaminophen may protect the gastric mucosa against ischemia-reperfusion injury, probably by blocking hydroxyl-radical-induced membrane damage.
我们研究了对乙酰氨基酚(一种解热镇痛药)对大鼠缺血再灌注诱导的急性胃黏膜损伤的影响。通过用小夹子夹住腹腔动脉30分钟来诱导缺血再灌注。再灌注60分钟后,测量糜烂总面积。在缺血前90分钟腹腔注射对乙酰氨基酚(300和500毫克/千克)可显著降低糜烂总面积。该药物还抑制了胃组织中缺血再灌注诱导的脂质过氧化物水平的升高以及体外羟基自由基(OH·)引起的脂质过氧化增加。在对照组和对乙酰氨基酚治疗组中,缺血再灌注后胃前列腺素E2(PGE2)含量均有升高趋势。对照组和对乙酰氨基酚治疗组之间胃PGE2含量未观察到显著差异。结果表明,对乙酰氨基酚可能通过阻断羟基自由基诱导的膜损伤来保护胃黏膜免受缺血再灌注损伤。