Impact of hepatic ischemia-reperfusion injury on kidney of rats

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(P0.05),γ-GT increased in I/R group(P0.05).The content of MDA in kidney increased in the 2 h,4 h reperfusion group with significantly higher than that in CTL group(P0.05).The Na~+-K~+-ATPase,Ca~(2+)-ATPase gradually decreased in I/R1h,I/R2h and I/R 4h group,compared with CTL,differences were statistically significant(P0.05).Compared with CTL,the content of ET in plasma increased in I/R1h,I/R2h,I/R4h group(P0.05),the content of ET in kidney increased in I group,I/R,I/R1h,I/R2h and I/R4h group(P0.05).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(P0.05).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.