论文部分内容阅读
目的 :研究血管紧张素转换酶抑制剂依那普利和血管紧张素 受体拮抗剂代文对于庆大霉素 (GM)肾损害的作用和机制。方法 :雄性 Wistar大鼠 40只 ,随机分为 4组 :1正常对照组 ;2 GM组 ;3GM+依那普利组 ;4GM+代文组。观察肾脏病理形态学变化 ,测定血、尿一氧化氮 (NO)、肌酐清除率 (CCr) ,尿 N 乙酰 βD 氨基葡萄糖苷酶 (NAG) ,尿蛋白 ,肾皮质匀浆中丙二醛 (MDA)、超氧化物歧化酶 (SOD)、一氧化氮合酶(NOS)等。结果 :应用依那普利的大鼠 ,GM肾损害的病理改变、CCr降低 ;尿中 NAG、蛋白增高等改变均加重 ;尿中 NO水平增加 ,血清 NO水平下降 ;肾皮质匀浆 NOS水平增高 ,SOD增高。应用代文的大鼠没有上述变化。结论 :依那普利通过 NO、活性氧代谢产物介导加重 GM肾毒性 ,而代文无此有害作用
AIM: To investigate the effects and mechanisms of enalapril and angiotensin receptor blocker (ACE) inhibitors on gentamicin (GM) renal damage. Methods: Forty male Wistar rats were randomly divided into 4 groups: 1 normal control group, 2 GM group, 3GM + enalapril group and 4GM + Daiwen group. The changes of renal pathomorphology were observed. The levels of serum and urine nitric oxide (NO), creatinine clearance (CCr), urinary N acetylglucosaminidase (NAG), urine protein and malondialdehyde ), Superoxide dismutase (SOD), nitric oxide synthase (NOS) and so on. Results: The rats with enalapril administration had decreased pathological changes of kidney and CCr, increased the levels of NAG and protein in urine, increased the level of NO in urine and decreased the levels of serum NO, and increased the levels of NOS in renal cortex homogenate , SOD increased. There was no such change in the application of siblings. CONCLUSIONS: Enalapril-mediated GM nephrotoxicity is mediated through NO and reactive oxygen metabolites, whereas de novo has the deleterious effect