【作者】 代红燕；

【导师】 张建龙；

【作者基本信息】 新疆医科大学 ， 病理学与病理生理学， 2007， 硕士

【摘要】 目的:观察大鼠肾缺血再灌注（I/R）损伤过程对脑的影响并探讨其可能的机制。方法:建立肾缺血再灌注损伤动物模型,按阻断血流不同时间再灌注1小时分为五组,即对照组、缺血30min再灌注60min组（IR30′+60′组）、缺血60min再灌注60min组（IR60′+60′组）、缺血90min再灌注60min组（IR90′+60′组）、缺血120min再灌注60min组（IRl20′+60′组）,每组8只。每组均测定血浆肌酐（Cr）、尿素氮（BUN）、丙二醛（MDA）的含量及谷胱甘肽过氧化物酶（GSH-PX）的活性;肾组织和脑组织中MDA的含量,GSH-PX、Na⁺-K⁺ATP酶、Ca²⁺-ATP酶、琥珀酸脱氢酶（SDH）的活性。结果:肾脏I/R导致肾脏明显的损伤,同时也导致脑损伤。随着肾缺血时间延长再灌注肾功能损害严重,血浆Cr、BUN含量、肾系数升高,差异有统计学意义（P＜0.05）;血浆、肾及脑组织脂质过氧化程度明显,自由基生成增多,MDA含量呈现上升趋势、GSH-PX活性呈现下降趋势,差异均有统计学意义（P＜0.05）。随着肾缺血时间延长再灌注,肾、脑组织能量代谢发生障碍,Na⁺-K⁺ATP酶、Ca²⁺-ATP酶和SDH活性有下降趋势,在缺血120min再灌注60min组下降明显。病理观察结果显示肾FR时,肾组织和脑组织有损伤性改变。结论:本实验复制的肾缺血再灌注损伤模型成功,结果提示肾缺血再灌注损伤过程可以引起脑组织脂质过氧化和脑细胞能量代谢障碍,甚至结构的改变。这可能是由于肾缺血再灌注损伤过程中所产生的自由基继发性造成脑组织脂质过氧化,并使清除自由基的酶活性减弱和生物氧化酶、Na⁺-K⁺ATP酶、Ca²⁺-ATP酶活性降低所致。更多还原

【Abstract】 Objective:To investigate the effect and mechanism on brain during kidney ischemiareperfusion injury of rats.Methods:A model of kidney I/R injury was established by imitation.Forty healthy male SD rats were randomly divided into 5 groups as following （n=8）:the control group（CTL,the group of sham operation）,60min reperfusion following ischemia 30min IR（30′+60′） group,60min reperfusion following ischemia 60min IR（60′+60′） group,60min reperfusion following ischemia 90min（IR（90′+60′） group）,60min reperfusion following ischemia 120minIR（120′+60′） group.In each group the rats were killed to obtain samples of kidney and brain at the specified time points.The contents of Cr,BUN,MDA,GSH-PX in blood、MDA,GSH-PX,SDH,ATPase in kidney and MDA,GSH-PX,SDH,ATPase in brain were observed in each group.Results:Kidney ischemia-reperfusion injury resulted in significant injury of kidney and brain.With the prolongation of ischemia,the function of Renal have obviously injury.The increase of BUN、Cr and kidney coefficient in blood have obviously statistic significance in IR（30′+60′） group（P＜0.05）,there were many free radical in blood,kidney and brain, the rising of MDA has statistic significance,the descent of GSH-PX has statistic significance（P＜0.05）.With the prolongation of ischemia,kidney and brain have disorder of energy metabolism.In IR（120′+60′） group,there have obviously decrease of Na⁺-K⁺ ATPase,Ca²⁺ATPase and SDH.There were change of injury in kidney and brain by pathological section.Conclusion:A model of kidney I/R injury was succeed.Kidney I/R injury can result in lipid peroxidation and disorder of energy metabolism,even change of structure in brain.The free radical were produced can result in lipid peroxidation of brain during the process of kidney I/R injury,at the same time,the decrease of enzymatic activity,these were main reasons.更多还原