中文摘要：

瞄准：调查胃的氧化应力和氮的氧化物的角色(没有) 在由在老鼠与的药的胃的出血性的侵蚀和他们的保护的形成是化学家 brain.METHODS：男 Wistar 老鼠为 24 h 被剥夺食物。在水合氯醛(300 mg/kg ) 下面麻醉，双边的颈动脉动脉结扎被执行。幽门和老鼠的颈动脉食管也被绑扎。胃然后与任何一个生理盐水为 3 h 被灌溉或模仿了加 17.4 mmol/L 胃朊酶和 54 mmol/L NaCl 包含 100 mmol/L HCl 的胃的果汁。老鼠被打死，胃被把。胃粘膜和胃的内容被收获。老鼠大脑被染色方法的 triphenyltetrazolium 为局部缺血的考试把。在胃的 ulcerogenic 参数变化，例如象提高的胃的酸背散开，粘膜类脂化合物过氧化物产生，组织安集中，钠血红素内容和粘膜一样的减少的粘膜谷胱甘肽水平在胃的样品的侵蚀，是 measured.RESULTS：双边的颈动脉动脉结扎在老鼠生产了严重大脑局部缺血(双性人) 。各种各样的 ulcerogenic 参数和粘膜的出血性的侵蚀的恶化在这些老鼠被观察。(P【0.05 ) 加重的 ulcerogenic 参数被抗氧化剂显著地稀释，例如外长的谷胱甘肽和 allopurinol。这些胃的参数被腹膜内氨基胍(100mg/kg ) 也改进，但是被 N (G)-nitro-L-arginine-methyl 酉旨加重(L 名字：25 mg/kg ) 。腹膜内 L 精氨酸(0-500 mg/kg ) dose-dependently 稀释了被 L-NAME.CONCLUSION 颠倒的 ulcerogenic 参数和出血性的侵蚀的导致双性人的恶化：双性人能通过精氨酸氮的氧化物小径的胃的氧化应力和激活生产出血性的侵蚀。

英文摘要：

AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats were deprived of food for 24 h. Under chloral hydrate （300 mg/kg） anesthesia, bilateral carotid artery ligation was performed. The pylorus and carotid esophagus of the rats were also ligated. The stomachs were then irrigated for 3 h with either normal saline or simulated gastric juice containing 100 mmol/L HCI plus 17.4 mmol/L pepsin and 54 mmol/L NaCI. Rats were killed and stomachs were dissected. Gastric mucosa and gastric contents were harvested. The rat brain was dissected for the examination of ischemia by triphenyltetrazolium chloride staining method. Changes in gastric ulcerogenic parameters, such as decreased mucosal glutathione level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples, were measured. RESULTS： Bilateral carotid artery ligation produced severe brain ischemia （BI） in rats. An exacerbation of various ulcerogenic parameters and mucosal hemorrhagic erosions were observed in these rats. The exacerbated ulcerogenic parameters were significantly （P〈 0.05） attenuated by antioxidants, such as exogenous glutathione and allopurinol. These gastric parameters were also improved by intraperitoneal aminoguanidine （100 mg/kg） but were aggravated by N^G-nitro-L-argininemethyl ester （L-NAME： 25 mg/kg）. Intraperitoneal L-arginine （0-500 mg/kg） dose-dependently attenuated BI-induced aggravation of ulcerogenic parameters and hemorrhagic erosions that were reversed by L-NAME. CONCLUSION： BI could produce hemorrhagic erosions through gastric oxidative stress and activation of arginine-nitric oxide pathway.