摘要
探讨缺血性急性肾功能衰竭的发病机理。选用大鼠一侧肾切除，对侧肾缺血６０分钟动物模型，观察再灌流前，再灌流后１５分钟，２４小时肾组织中超氧化物歧化酶（ＳＯＤ）（包括总ＳＯＤ、锰ＳＯＤ和铜锌ＳＯＤ）和丙二醛（ＭＤＡ）含量的变化及还原型谷胱甘肽（ＴＡＤ）对它们的影响。结果发现，６０分钟肾缺血和再灌流可致肾组织中三种ＳＯＤ活性呈进行性显著降低，再灌流１５分钟、２４小时肾组织中ＭＤＡ含量呈进行性显著增高。给ＴＡＤ能显著减轻肾组织中ＭＤＡ含量的增高，但对降低的ＳＯＤ无影响。结果提示：肾缺血和再灌流可造成肾组织对氧自由基清除能力显著降低，肾组织发生脂质过氧化损伤，ＴＡＤ能显著减轻肾脂质过氧化损伤，线粒体损伤可能是肾脂质过氧化进行性加重的主要因素。
Toinvestigatethemechanismofischemicacuterenalfailure.Theratrenalischemiamodelwithrightnephroectomyandoclusionoftheleftrenalpediclefor60minuteswasusedinthisexperiment.ThechangesofSOD(superoxidedismutase)includingtotalSOD、Mn-SODandCu-Zn-SODandMDA(Malondialdehyde)intherenaltisueandefectsofTAD(reducedglutathione)onthemwerestudiedatthetimeofOmin、15min、24hreper-fusionafter60minrenalischemia.Wefoundthat60minischemiaandreperfusioncanresultinaremarkablere-ductionofalthreeSODintherenaltisue.TherenaltissueMDAlevelincreasedevidentlyafterthereperfusionfor15minor24h.TADcanrelievetheMDAincreasingdegreintherenaltissueatthesametime.Theseresultssuggestedthattherenalischemiaandreperfusioncanresultinthattheabilityofrenaltissuetoclearfreeradicalsdecreasedandtherenaltisuesuferedlipidperoxidation.TADcanrelievetherenaltisuelipidperoxidation.Theinjuryofmitochondriamaybeanimportantfactorthatmakesrenaltissuelipidperoxidationaggravated.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
1996年第2期72-75,共4页
Chinese Journal of Nephrology
