缺血性损伤对肝移植胆道微循环的影响及重组人生长激素的保护作用

目的：探讨大鼠肝移植胆道缺血性损伤对肝内胆道微循环的影响及重组人生长激素的保护作用。方法：建立大鼠自体原位肝移植模型，随机分为3组（每组6只）：对照组（CON），胆道缺血性损伤组（HAL），重组人生长激素（rhGH）处理组。于术后7d取肝组织，用兔抗CD34多克隆抗体标记血管，光镜下观察汇管区血管、胆管并计数。结果：HAL组肝内胆管上皮细胞排列明显缺失，汇管区无明显炎症细胞浸润，汇管区血管及胆管数明显减少，不伴有血管的胆管数明显增多（P〈0．05）；rhGH处理组肝内胆管上皮细胞呈慢性增生性炎症改变，汇管区血管及胆管数增加，伴有血管的胆管数明显增多（P〈0．05）。结论：大鼠自体原位肝移植胆道缺血性损伤使肝内胆道微循环受损，而外源性rhGH促进肝内胆道微循环的恢复从而对胆道有保护作用。

Effect of ischemia injury on microcirculation of bile ducts relating to liver transplantation and protective effect of recombinant human growth hormone

AIM： To investigate the changes of microcirculation of bile ducts relating to liver transplantation in rats with ischemia injury and protective effect of recombinant human growth hormone （rhGH） on ischemia injury. METHODS： The rat orthotopic autologous liver transplantation was performed firstly. Wistar rats were randomly divided into three groups each with 6 rats including control group （CON）, ischemia injury group （HLA）and rhGH group. Specimen of liver tissue was collected after The blood vessels were tagged 7 days post-operation. with rabbit anti-CD34 polyclonal antibody. The blood vessels and bile ducts of portal area were observed and enumerated. RESULTS： In HAL group, the array of intrahepatic cholangiocytes was significantly absent. There was no obvious soakage of inflammatory cells in portal area. The number of blood vessels and bile ducts in portal area was significantly decreased. The number of bile ducts not accompanying with blood vessels was significantly increased （P 〈 0.05 ）; In rhGH group, the changes of chronic hyperplastic inflammation were oberserved in intrahepatic cholangiocytes. The number of blood vessels and bile ducts in portal area was significantly increased. The number of bile ducts accompanying with blood vessels was significantly increased （ P 〈 0.05）. CONCLUSION： Ischemia injury of bile duets relating to rat orthotopic autologous liver transplantation damnifies the microeirculation of intrahepatic bile ducts. However, administration of exogenous rhGH promotes recovery of intrahepatic microeirculation consequently protecting bile duets from ischemia injury.