大鼠肝脏__

大鼠肝脏缺血再灌注损伤对肾的影响

http://www.100md.com 《新疆医科大学学报》 2006年第8期

大鼠肝脏,,肝脏；缺血再灌注损伤；肾脏；内皮素；血管紧张素Ⅱ；醛固酮,1材料与方法,2结果,3讨论,参考文献:

     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 h、I/R 2 h、I/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(γGT)、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。

    关键词：肝脏；缺血再灌注损伤；肾脏；内皮素；血管紧张素Ⅱ；醛固酮

    Impact of hepatic ischemiareperfusion injury on kidney of ratsSUN Zhan, WANG Hongmei, ZHANG Jianlong, et al

    (Department of Pathophysiology, Preclinical College, Xinjiang Medical University,

    Urumqi 830054, China)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. ......

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