中文摘要：

目的将在老鼠在胆汁 canalicular F 肌动朊微细丝上调查肝的 ischemia-reperfusion (I/R ) 的效果。肝的 ischemia-reperfusion 的方法 A 老鼠模型被雇用，局部缺血时间是 35 min。浆液丙氨酸 aminotransferase (中高音) 的活动， aspartate aminotransferase (著名计算机生产厂商) ， γ； -glutamyl transferase (GGT ) 和全部的 bilirubin (TBIL ) 的水平被测量。在胆汁 canaliculi 的变化被传播电子显微镜观察。F 肌动朊微细丝的修正被使用 FITC-Phalloidin 确定并且由扫描显微镜学成像的共焦的激光分析了。染色的 F 肌动朊的结果修正与观察由传播电子显微镜学做了一致。染色 F 肌动朊在在灌注前的 hepatocytes 是正常的，但是在灌注以后显著地减少了，并且有 canalicular 的显著损失在灌注以后的微绒毛，它与反常浆液 GGT 和 TBIL 层次与一致。结论灌注，不是短期的局部缺血，导致了 F 肌动朊微细丝的混乱和微绒毛的损失。这些修正能由损坏 canalicular 收缩导致损害胆汁分泌物，并且能是在在老鼠的肝的 ischemia-reperfusion 以后的 cholestasis 的主要机制。

英文摘要：

Objective：To investigate the effect of hepatic ischemia-reperfusion（I/R） on bile canalicular F-actin microfilaments in rats. Methods： A rat model of hepatic ischemia-reperfusion was employed and the ischemia time was 35 min. The activity of serum alanine aminotransferase （ALT）, aspartate aminotransferase（AST）, γ-glutamyl transferase（GGT） and the level of total bilirubin（TBIL） were measured. Changes in the bile canaliculi were observed by transmission electron microscope. The modification of F-actin microfilaments was quantified by using FITC-Phalloidin and analyzed by confocal laser scanning microscopy imaging. Results：Modifications of F-actin staining were consistent with the observations made by transmission electron microscopy. The staining of F-actin was normal in hepatocytes before reperfusion but decreased significantly after reperfusion, and there was a marked loss of canalicular microvilli after reperfusion, which coincided with abnormal serum GGT and TBIL levels. Conclusion：Reperfusion, not short-term ischemia, induced a disruption of F-actin microfilaments and a loss of microvilli. These modifications could lead to the impaired bile secretion by damaging canalicular contraction, and could be the main mechanisms of cholestasis after hepatic ischemia-reperfusion in rats.