裴秋玲 王冬梅 姜妙娜 贾玉杰 裴德恺 黄辰格 116027,大连医科大学公共卫生学院. 中华肝脏病杂志 1999 0 7 1


    关键词：胆汁淤积，肝内 一氧化氮 大鼠 期刊 zhgzbzz 0 基础研究 fur -->


    

摘要 目的 探讨肝内胆汁淤积时NO与胆淤生物化学变化关系。方法 利用ANIT诱发大鼠肝内胆汁淤积的模型，动态观察内源性NO、肝内胆汁淤积生物化学改变、肝组织线粒体功能和肾排泄的变化。结果 IC大鼠模型早期肝内胆汁淤积，血清胆红素、ALT、AKP和胆酸明显升高，伴随血NO升高和肾排泄增加。肝组织NO增高和肝线粒体SDH活性下降持续至观察中期，且两者呈负相关(r=-0.92)。结论 该模型肝组织NO增加可能参与肝内胆汁淤积损伤过程；血清胆红素迅速下降，胆酸、ALT和AKP降至正常水平可能和血NO增高介导肾排泄增多有关。

    

Dynamic changes of nitric oxide andbiochemistry in rats with intrahepatic cholestasis

PEI Qiuling,WANG Dongmei,JIANGMiaona,et al.

Dalian Medical University,Dalian 116027

Abstract Objective Toinvestigate the correlation between nitric oxide and biochemical changes of intrahepaticcholestasis.Methods Studies were made on endogenous NO,biochemicalchanges of cholestasis,liver mitochondrial function and renal excretion in a rat model atdifferent time points after ANIT administration.Results In acute reactivephase,serum bilirubin,ALT,AKP,and bile acids significantly increased,accompanied byenhanced plasma NO and renal excretion.Liver NO increased and mitochondrial SDH activitydecreased for 2-6 days after ANIT.There was a high negative correlation between liver NOand mitochondrial SDH activity (r=-0.92).Conclusion These results showthat higher liver NO may be an important mediator of intrahepaticcholestasis.However,plasma NO increase may play a role in rapidly decreasing serumbilirubin and restoring bile acids,ALT,and AKP to control levels by mediating enhancedrenal excretion.

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