小剂量多巴胺在肾缺血-再灌注损伤中的抗损伤作用

Effect of Low Dose Dopamine on Renal Ischemia-Reperfusion Injury

目的探讨多巴胺在抗肾缺血-再灌注中损伤中的作用及其可能的作用机制.方法选取体质量(2.1±0.2)kg的日本大耳白兔23只,随机分为生理盐水对照组(n=11)和多巴胺组(n=12),采用双盲法,通过夹闭家兔肾动脉的方式建立肾缺血模型,两组家兔在实验过程中分别持续静滴生理盐水或多巴胺1.5～2μg/(kg.min).分别于夹闭肾动脉前和缺血50min再灌注30min后取家兔肾静脉血,检测血肌酐(Sc)r、血尿素氮(BUN)和丙二醛(MDA),并记录缺血再灌注前后的尿量.结果两组血肌酐、血尿素氮和丙二醛在再灌注后较夹闭前均明显升高(P<0.05);再灌注30min后对照组各指标升高更明显(P<0.05),而尿量无明显统计学差异(P>0.05).结论小剂量多巴胺对肾缺血-再灌注损伤具有抗损伤保护作用,其作用机制可能与抗氧化作用有关.

Objective To investigate the effect and mechanism of dopamine on renal ischemia-reperfusion injury in rabbits. Methods Twenty-three rabbits （either gender, weighing （2.1 ＋0.2） kg were randomly divided into dopamine group （n = 12） and control group （n = 11） , double- blind trial was used. The rabbit ischemia-reperfusion injury model was established by clamping renal artery for 50min and reperfusion for 30 min, Dopamine injection was administered intravenously1.5 - 2 μg/（kg.min）during the whole renal ischemia-reperfusion in dopamine group.In control group an equal amount of 0.9 % sodium chloridate solution was given. Concentrations of serum creatinine （Cr） , blood urea nitrogen （BUN） , malondialdehyde （MDA） , urine volume before clamping renal artery and 30 min after reperfusion were measured respectively. Results Levels of Cr, BUN and MDA increased at 30 min after reperfusion compared with before clamping within group respectively （P 〈 0.05 ）. Cr, BUN and MDA in dopamine group were significantly lower than those in control group at 30min after reperfusion （P 〈 0.05 ）. There was no statistical difference in urine volume between the two groups （P 〉 0.05）.Conclusions Low dose dopamine is effective in preventing renal ischemia-repeffusion injury in rabbits. The mechanism underlying the protective effect may be associated with its anti-oxidative activity.