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目的 :探讨一氧化氮 (NO)在兰索拉唑对大鼠胃粘膜保护中的作用。 方法 :在乙醇诱导大鼠胃粘膜损伤前 ,预先给予兰索拉唑 (2 0 m g/ kg)灌胃 ,L-硝基 -精氨酸甲酯 (L- NAME,4m g/ kg)、L-精氨酸 (2 5 0 mg/ kg) ,D-精氨酸 (2 5 0 m g/ kg)静脉注射。测定胃粘膜血流量 (GMBF)、胃液 p H、胃粘膜和血浆的 NO2 - / NO3- ,并观察了胃粘膜损伤指数 (ulcer index,UI)、溃疡坏死组织和中性粒细胞浸润程度的变化。结果 :与模型损伤组相比 ,兰索拉唑组大鼠 U I明显降低 (P<0 .0 1) ,溃疡坏死组织和中性粒细胞浸润程度明显减轻 (P<0 .0 1)。用 L- NAME处理后 ,兰索拉唑保护胃粘膜损伤作用明显减弱 ;L- NAME抑制作用可被 L-精氨酸拮抗 ,而不被 D-精氨酸拮抗。向胃内灌注兰索拉唑 ,可增加 GMBF、胃粘膜和血浆的 NO2 - / NO3- ,L- NAME可逆转这种作用 ,但对兰索拉唑抑制酸分泌作用无明显影响。 结论 :兰索拉唑对大鼠胃粘膜保护作用与 NO有关 ,而兰索拉唑抑制酸分泌作用与 NO无关。
Objective: To investigate the role of nitric oxide (NO) in gastric mucosal protection in rats. Methods: Before ethanol-induced gastric mucosal lesion in rats, Lansoprazole (20 mg / kg), L-NAME (4 mg / kg), L - arginine (250 mg / kg), D-arginine (250 mg / kg) intravenously. Gastric mucosal blood flow (GMBF), gastric juice p H, gastric mucosa and plasma NO 2 - / NO 3- were measured and the changes of ulcer index (UI), ulcer necrosis tissue and neutrophil infiltration were observed . Results: Compared with the model group, the U 1 level in the lansoprazole group was significantly lower (P <0.01), and the degree of infiltration of necrotic tissue and neutrophil in the ulcer group was significantly reduced (P <0.01). L-NAME treatment, lansoprazole protective effect of gastric mucosal injury was significantly weakened; L-arginine inhibition can be L-arginine, but not D-arginine antagonism. Lansoprazole infused into the stomach increased NO2 - / NO3- in GMBF, gastric mucosa and plasma. L-NAME reversed this effect, but had no obvious effect on the inhibition of acid secretion by lansoprazole. Conclusion: The protective effect of lansoprazole on gastric mucosa in rats is related to NO, while the inhibition of acid secretion by lansoprazole is not related to NO.