Objective:To explore the roles of peribiliary vascular plexus(PBP) on regeneration of intrahepatic bile ducts after warm ischemia-reperfusion injury and the possible meshanism of PBP on bile ducts sensitive to warm ischemia-reperfusion injury of transplanted liver.
Methods :Male SD rats were used in this experiment. The animals were divided into three groups: shame operation group（S group）, warm ischemia of grafts for 0 min group (W0 group),and warm ischemia of grafts for 10 min group (W10 group). Seven time points were determined as 0 h,6,24 h,and 3,7,14,30 d post-reperfusion. Six animals were used per time-point. ALT, GGT, and TBIL of serum were determined.Serial liver sections were made and were immunolocalized by CK19 and FⅧ-R Ag to assess the co-localization of bile ducts and microvessels. Bile ducts were identified by CK19 and microvessels were identified by FⅧ-R Ag.
Results:In W10 group, the level of plasma GGT and total bilirubin was elevated with a increase longer than in W0 group. The portal inflammation, damage of bile ducts,and fibrosis area of portal area of W10 group were significantly more seriously than those in W0 and S groups. Under electron microscope, micro-thrombosis in microvessels were observed in W10 group. Furthermore, in W10 group, the number of intraportal microvessels at 6h and 24 h post-reperfusion was markedly decreased compared to that of W0 and S groups. In W10 group, although cholangiocytes showed significant regeneration at 24 h post-reperfusion, the number of intraportal microvessels and bile ducts with accompanying microvessels was not higher than that of W0 and S groups at 14 to 30 days after reperfusion.
Conclusions:Warm ischemia-reperfusion injury of liver grafts can cause microthrombosis of peribilary vascular plexus and induce increased damage of vascular endothelial cells and the later can cause disturbance of microcirculation of bile ducts and delayed regcneration of bile ducts.These changes may be important causes of vulnerability of bile ducts to warm ischemia-reperfusion injury.