缺血再灌注肾血管反应性损伤中的作用
肾,,]肾;缺血再灌注损伤;离体灌流肾;过氧亚硝基阴离子;氨基胍;肾血管反应性;大鼠,1材料与方法,2结果,3讨论,[参考文献]
[摘要]目的 探讨过氧亚硝基阴离子(ONOO-)在大鼠缺血再灌注肾血管反应性损伤中的作用。方法 应用离体灌流肾(isolated perfused kidney, IPK)技术观察肾缺血再灌注(ischemia reperfusion,IR)后肾血管对去甲肾上腺素(norepinephrine,NE)和乙酰胆碱(acetylcholine,Ach)反应性的改变;观察应用氨基胍(aminoguanidine,AG)阻断内源性NO生成对肾IR大鼠IPK肾血管反应性的影响,以及给予外源性ONOO-后大鼠IPK肾血管反应性的改变。结果 IR后IPK肾血管对NE的缩血管反应性和对Ach的舒血管反应性都有明显降低,IR5h较IR1h进一步降低(均P<0.01)。ONOO-(40μmol·L-1)与vehicle相比则显著降低IPK肾血管对NE和Ach的反应性(均P<0.01)。AG+IR1h组大鼠IPK肾血管对NE和Ach的反应性与NS(生理盐水)+IR1h组大鼠相比无显著差异(均P>0.05),AG+IR5h组大鼠肾血管对NE和Ach的反应性较NS+IR5h组明显增强(均P<0.05)。结论 ONOO-在肾IR所致的肾血管反应性损伤中具有重要的作用。[关键词]肾;缺血再灌注损伤;离体灌流肾;过氧亚硝基阴离子;氨基胍;肾血管反应性;大鼠
Effects of peroxynitrite on renal vascular response in isolated
perfused kidney after rats renal ischemia reperfusionWANG Xinliang1, DUAN Guowei 2, XUE Xiaoying2,LI Hongjuan1
(1. Department of Pediatrics, the Second Hospital, Hebei Medical University, Shijiazhuang 050000, China; 2. Department
of Radiotherapy, the Second Hospital, Hebei Medical University, Shijiazhuang 050000, China) Abstract:Objective To investigate the effects of peroxynitrite(ONOO-) on renal vascular response in isolated perfused kidney(IPK) after renal ischemia reperfusion(IR). Methods IPK was used to examine the effects of renal IR on renal vascular response, the effects of iNOS inhibition on the renal vascular response changes caused by renal IR, and the effects of administration of ONOO- on above parameters. Results Contractile response of renal vascular to norepinephrine(NE) and relaxation responses of renal vascular to acetylcholine(Ach) both were depressed obviously, IR5h was overdepressed compared with IR1h (all P<0.01). ONOO-(40μmol·L-1)depressed notably the renal vascular response to NE and Ach compared with vehicle (all P<0.01). The renal vascular response to Ach and NE was not effected in IR1h by AG, but was strengthened in IR5h (all P<0.05). Conclusion it is proved in IPK model that the generation of ONOO- possesses important role in renal vascular response damage of rats after renal IR. ......
您现在查看是摘要页,全文长 14084 字符。