摘要
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增高介导紧排泄增多有关。
Objective To investigste the correlation between nitric oxide and biochemical chances ofintrahepatic cholestasis. Methods Studies were made on endogenous NO, biochemical changes ofcholestasis, liver mitochondrial function and renal excretion in a rat model at different time points afterANIT administration. Results in acute reactive phase, serum bilirubin, ALT, AKP, and bile acidssignificantly increased, accompanied by enhanced plasma NO and renal excretion. Liver NO increased andmitochondrial SDH activity decreased for 2-6 days after ANIT. There was a high negative correlationbetween liver NO and mitochondrial SDH activity (r=-0.92). Conclusion These results show that higherliver NO may be an important mediator of intrahepatic cholestasis. However, plasma NO increase mayplay a role in rapidly decreasing serum bilirubin and restoring bile acids, ALT, and AKP to control levelsby mediating enhanced renal excretion.[
出处
《中华肝脏病杂志》
CAS
CSCD
1999年第1期44-45,共2页
Chinese Journal of Hepatology
关键词
胆汁淤积
一氧化氮
生物化学
]: Cholestasis
intrahepatic
Nitric
oxide
Rats
