引用本文:王新良,段惠军,陈晓玲,黄善生.NO、ONOO-在大鼠离体肾缺血再灌注肾功能损伤中的作用[J].大连医科大学学报,2005,27(4):263-267.
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NO、ONOO-在大鼠离体肾缺血再灌注肾功能损伤中的作用
王新良1, 段惠军2, 陈晓玲3, 黄善生3
1.河北医科大学 第二医院 儿科,河北 石家庄 050000;2.河北医科大学 病理解剖学 教研室,河北 石家庄 050017;3.河北医科大学 病理生理学教研室,河北 石家庄 050017
摘要:
[目的]探讨一氧化氮(nitric oxide,NO)、过氧亚硝基阴离子(peroxynitrite ,ONOO-)在大鼠离体肾缺血再灌注损伤时对肾功能的影响。[方法]应用离体灌流肾(is olated perfused kidney,IPK)技术观察肾I-R对菊粉清除率(Cin)、尿钠排泄指数(FENa )、 肾血管阻力(RVR)的影响;阻断内源性NO生成对肾I-R所致的上述指标变化的影响;外源性 直接给予NO供体硝普钠(SNP)、ONOO-对大鼠IPK肾功能的影响。[结果]①缺血再灌注 导 致大鼠IPK肾血管阻力(RVR)明显增大(P<0.05),IPK的Cin降低(P<0.05),肾 I-R后IPK的FENa有较大幅度的增加(P<0.05)。②SNP能够使健康大鼠IPK的RVR降低、C in增加和FENa增大(P<0.05)。而ONOO-使RVR增高、Cin降低和FENa增加(P<0.0 5)。③iNOS抑制剂氨基胍(aminoguanidine,AG)使大鼠IPK的功能I-R后5 h RVR降低、Ci n增大和尿钠减少(P<0.05);而应用NOS抑制剂N-硝基-L-精氨酸(L-NNA),加重了肾 I-R大鼠IPK肾机能的损伤,I-R1h和I-R 5 h均出现了RVR增大、Cin降低和尿钠排泄增多(P<0.05)。[结论]肾I-R所致NO大量生成后产生的ONOO-损伤了大鼠的肾功能。
关键词:    缺血再灌注损伤  离体灌流肾  一氧化氮  过氧亚硝基阴离子  氨基胍  肾功能
DOI:10.11724/jdmu.2005.04.05
分类号:R692.5
基金项目:
Effects of nitric oxide and peroxynitrite on renal function in isolated perfused kidney after renal I-R
WANG Xin-liang1, DUAN Hui-jun2, CHEN Xiao-ling3, HUANG Shan-sheng3
1.Department of Pediatric of Second Hospital, Hebei Medical University, Shijia zhuang 050000, China;2.Department of Pathology, Hebei Medical University, Shij iazhuang 050017, China;3.Department of Pathophysiology, Hebei Medical University , Shijiazhuang 050017, China
Abstract:
[Objective]To investigate the effects of nitric oxi de (NO) and peroxy nitrite on renal function in isolated perfused kidney(IPK) after renal I-R. [Me thods]Isolated perfused kidney (IPK) was used to examine the effects of renal I -R on renal vascular resistance (RVR), glomerular filtration rate (GFR), fractio nal excretion of sodium (FENa); and the effects of NOS inhibition on the changes of those parameters caused by renal I-R; and the effects of SNP and ONOO- on the changes of those parameters caused by renal I-R.[Results]①RVR was increas ed, GFR was decreased, FENa was enhanced after renal I-R(P<0.05)in IPK.②S NP results in reduction of RVR, increasing of Cin and increment of FENa(P<0. 05). ONOO- (40 μmol/L) caused RVR heightened, Cin decreased and FENa increase d(P<0.05). ③RVR reduced、Cin increased and FENa enhanced(P<0.05) in I-R 5h i n IPK given AG; but L-NNA aggravated the renal injuries caused by renal I-R, exh ibited augmented R VR, reduced Cin and enhanced FENa both in I-R1h and I-R5h(P<0.05).[Conclusi on]It is proved in IPK model that a massive quantity of NO and the generation o f ONOO- play important role in renal damage of rats after renal I-R.
Key words:  renal  ischemia reperfusion  isolated perfused kidn ey  nitric oxide  peroxynitrite  aminoguanidine  renal function