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作 者:王新良[1] 段惠军[2] 陈晓玲[3] 黄善生[3]
机构地区:[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
出 处:《大连医科大学学报》2005年第4期263-267,共5页Journal of Dalian Medical University
摘 要:[目的]探讨一氧化氮(nitricoxide,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(isolatedperfusedkidney,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、Cin增加和FENa增大(P<0.05)。而ONOO-使RVR增高、Cin降低和FENa增加(P<0.05)。③iNOS抑制剂氨基胍(aminoguanidine,AG)使大鼠IPK的功能I-R后5hRVR降低、Cin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-R5h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。[ Objective] To investigate the effects of nitric oxide (NO) and peroxynitrite on renal function in isolated perfused kidney(IPK) after renal I- R. [ Methods] Isolated perfused kidney (IPK) was used to examine the effects of renal I- R on renal vascular resistance (RVR), glomerular filtration rate (GFR), fractional 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 increased, GFR was decreased, FENa was enhanced after renal I- R( P 〈 0. 05)in IPK. ②SNP 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 increased( P 〈 0. 05). ③ RVR reduced, Cin increased and FENa enhanced ( P 〈 0.05) in I-R 5h in IPK given AG; but L - NNA aggravated the renal injuries caused by renal I - R, exhibited augmented RVR, reduced Cin and enhanced FENa both in I - R 1 h and I - R 5h ( P 〈 0. 05). [ Conclusion] It is proved in IPK model that a massive quantity of NO and the generation of ONOO^- play important role in renal damage of rats after renal I-R.
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