摘要
目的 探讨NO在脂多糖 (LPS)诱导肝硬化大鼠肾功能障碍中的作用。方法 采用复合因素复制肝硬化模型 ,至 8周末 ,将其分为 3个组 :Ch +NS(肝硬化对照组 )、Ch +L Arg(精氨酸组 )和Ch +LNNA(LNNA组 ) ,分别用生理盐水 1 5ml、L Arg 10 0mg·kg-1·d-1和LNNA 2 0mg·kg-1·d-1灌胃 ,共 2周 ,同时有LPS(脂多糖对照组 )和NS(正常对照组 )。于处死大鼠前 4h ,腹腔内注射LPS 3mg/kg诱发肝硬化大鼠肾功能障碍。观察血清NO及肾功能的改变。 结果 血清醛固酮水平在Ch+LNNA组最高 ,Ch +L Arg组最低 ;尿钠排泄量在Ch +LNNA组明显低于其他各组 ;肌酐清除率在Ch +LNNA组最低 ,Ch+L Arg组明显高于Ch +NS组。 结论 NO可能通过舒张血管、拮抗内皮素等而改善肾循环 。
Objective To explore the effect of nitricoxide on renal dysfunction in cirrhotic rats induced by lipopolysaccharide(LPS). Methods The cirrhotic model of Wistar rats was established by complex pathogens. After 8 weeks the rats reached mid and late stage cirrhosis and were divided into Ch+NS, Ch+L Arg and Ch+LNNA groups, which were intragastric infused with normal saline (1 5 ml/d), L Arg(100 mg·kg -1 ·d -1 ) and LNNA (20mg·kg -1 ·d -1 ) respectively for 2 weeks. Besides LPS and NC (normalcontrol) groups were set. The renal dysfunction in cirrhotic rats were inducedby a dose of 3 mg/kg LPS injected in peritoneal cavity at hour 4 before the ratswere sacrificed. The level of plasma NO and renal function were detected. Results The level of serum aldosterone was the highest in Ch+LNNA group, but thelowest in Ch+L Arg group. The urine sodium excretion (UNaV) was markedly lowerin Ch+NS and Ch+LNNA groups than in other groups. The creatinine clearance (CrC) was significantly higher in Ch+L Arg group than in Ch+NS group, and was the lowest in Ch+LNNA group. Conclusion NO may inhibit the development of renaldysfunction by vasodilatation and antagonizing endothelin, improving renal microcirculation.
出处
《山西医科大学学报》
CAS
2003年第1期13-15,共3页
Journal of Shanxi Medical University
基金
山西省卫生厅科技发展计划项目 (2 0 0 14 0 )
