【摘要】 目的:探讨大鼠肝脏缺血再灌注(I/R)损伤对肾的影响及可能的机制。方法:Wistar大鼠48只,随机分为对照组(假手术组)、缺血30 min组(I组)、缺血30 min再灌注组(I/R组)及缺血30 min再灌注后1、2、4 h组(I/R 1 hI、/R 2 hI、/R 4 h组),测定各组血清中谷氨酰转移酶(GTP)、碱性磷酸酶(AKP)、γ-谷氨酸转肽酶(-γGT)、尿素氮(BUN)、肌酐(Cr)含量及肾组织中丙二醛(MDA)含量和Na+-K+-ATP酶、Ca2+-ATP酶的活性,并测定血清和肾组织血管紧张素Ⅱ(AngⅡ)、醛固酮(Ald)、内皮素(ET)的含量。结果:肝脏I/R导致肝脏、肾脏明显损伤,表现I/R各组血清GTP、AKP、γ-GT、BUN、Cr含量明显高于对照组(P<0.05);与对照组相比,I/R 1、2、4 h组肾组织MDA、ET含量明显升高,Na+-K+-ATP酶、Ca2+-ATP酶活性明显降低(P<0.05),血清ET含量明显升高(P<0.05),I/R 2、4 h组血清AngⅡ含量明显高于对照组(P<0.05);与对照组相比,其余各组肾组织中AngⅡ的含量均明显升高(P<0.05),I/R及I/R 1、2、4 h组血清和肾组织中Ald含量均明显高于对照组(P<0.05),随着肝脏I/R后时间的延长,肝脏出现炎性细胞浸润,肝细胞片状坏死,肾小球、肾小管细胞水肿、充血。结论:肝脏I/R损伤可造成肾功能损伤,损伤机制在自由基损伤的基础上,与肾素-血管紧张素-醛固酮系统有关。更多还原

【Abstract】 Objection: To investigate the impact of hepatic ischemia-reperfusion on kidney of rats.Methods: A model of liver I/R injury was established by imitation.Forty-eight healthy Wister rats were randomly divided into 6 groups as following（n=8）: the control group（CTL,the group of sham operation）,simply ischemia 30min without reperfusion（I group）, reperfusion following ischemia 30 min（I/R group）,1 hour reperfusion following ischemia 30 min（I/R1h）,2 hours reperfusion following ischemia 30min（I/R2h） and 4 hours reperfusion following ischemia 30 min（I/R4h）.In each group the rats were killed to obtain samples of kidney at the specified time points.The contents of GTP,AKP,γ-GT,BUN,Cr in blood and MDA in kidney were observed in each group.The contents of angiotoninⅡ（AngⅡ）,aldosterone（Ald） and endothelin （ET） in plasma and kidney were measured by radioimmunity.Results: Hepatic ischemia-reperfusion resulted in significant kidney injures.With the extension of ischemia-reperfusion,comparing with CTL,BUN and Cr in blood increased significantly in I group（P<0.05）,γ-GT increased in I/R group（P<0.05）.The content of MDA in kidney increased in the 2 h,4 h reperfusion group with significantly higher than that in CTL group（P<0.05）.The Na⁺-K⁺-ATPase,Ca²⁺-ATPase gradually decreased in I/R1h,I/R2h and I/R 4h group,compared with CTL,differences were statistically significant（P<0.05）.Compared with CTL,the content of ET in plasma increased in I/R1h,I/R2h,I/R4h group（P<0.05）,the content of ET in kidney increased in I group,I/R,I/R1h,I/R2h and I/R4h group（P<0.05）.Compared with CTL,the content of AngⅡ in plasma increased in I/R2h,I/R4h group（P<（0.05））,the content of AngⅡ in kidney increased in I,I/R,I/R1h,I/R2h,I/R4h group（P<0.05）.Aldosterone in plasma and kidney increased in I/R,I/R1h,I/R2h,I/R4h group compared with CTL（P<（0.05））.Conclusion: Liver ischemia-reperfusion can induce injury to kidney in the early stage of reperfusion.The results suggested that renin angiotensin aldosterone system involved in the forming of kidney tissue injury after liver ischemia-reperfusion underlying the oxygen free radicals damage.更多还原