中文摘要：

在临床的肝移植的背景，肝的动脉的 ischaemia 的延期是否增加胆汁的纤维变性，是争论的。我们设计了一个肝移植模型测试这争吵并且探索它的机制。12 条狗随机被划分成二个组的方法：肝的动脉的 ischaemia (HAI ) 和控制组。在 HAI 组，肝的动脉被酒在门灌注以后的 60 分钟，但是在控制组，，肝的动脉的灌注与门灌注是同时的。intrahepatic 胆汁管的病理学的变化被观察。转变生长因素贝它 1 (TGF-1 ) ，在 intrahepatic 胆汁管的上皮的房间表示了，被 immunohistochemical streptoadividin-biotin 检测复杂方法。Smad3， P-Smad3 和 alpha 的 transcriptional 层次的表达式弄平肌肉肌动朊(在 intrahepatic 胆汁管的 -SMA) mRNA 被与控制组，更多的骨胶原免职和 leucocytic 渗入相比的西方的弄污和 RT-PCR respectively.Results 检测能在胆汁的容器墙中被看见。显著地，更多的 buffy 粒子，是 TGF-1 的蛋白质，能在胆汁的上皮的房间被看见。P-Smad3 和 -SMA mRNA (作为到在 intrahepatic 的相应 -actin) 的比率，胆汁管是 1.82

英文摘要：

Background In clinical liver transplantation, whether the delay of hepatic arterial ischaemia increases biliary fibrosis or not is controversial. We designed a liver transplantation model to test this controversy and explore its mechanism. Methods Twelve dogs were divided into two groups randomly： hepatic arterial ischaemia （HAI） and control groups. In HAI group, hepatic artery was perfused 60 minutes after portal perfusion, but in control group, hepatic arterial perfusion was simultaneous with portal perfusion. The pathological changes of intrahepatic bile ducts were observed. Transforming growth factor beta 1 （TGF-β1）, expressed in epithelial cells of intrahepatic bile duct, was detected by immunohistochemical streptoadividin-biotin complex method. Expressions of Smad3, P-Smad3 and the transcriptional levels of alpha smooth muscle actin （α-SMA） mRNA in intrahepatic bile ducts were detected by Western blotting and RT-PCR respectively.Results Compared with the control group, more collagen deposition and leucocytic infiltration could be seen in biliary vessel walls. Significantly more buffy particles, which are the proteins of TGF-β1, could be seen in biliary epithelial cells. P-Smad3 and α-SMA mRNA （as ratio to corresponding β-actin） in intrahepatic bile ducts were 1.82±0.18 and 1.86±0.73 respectively in HAI group, significantly higher than those in control group （0.59±0.09 and 0.46±0.18, respectively）. Conclusions Hepatic arterial ischaemia could increase the deposition of collagen fibres, trigger the transdifferentiation of myofibroblasts in intrahepatic bile duct and might result in biliary fibrosis by activating the TGF-β1 signalling pathway.