胆道铸型综合征动物模型的建立

Establishment of animal model for biliary cast syndrome

目的建立胆道铸型综合征的动物模型，探讨胆道铸型综合征发生的病理机制。方法40只日本大耳白兔被随机分成两组，实验组用石炭酸腐蚀肝内外胆道上皮，后以支撑管连接；对照组（假手术组）仅作肝外胆道的横断及支撑管连接。术后观察4周后处死，行肝脏大体标本解剖及病理切片分析。结果全部兔均按预期方案手术成功，在随后的观察期内，实验组有6只兔在术后3周左右死亡，实验组及对照组在观察期均出现精神萎靡、食欲不振、大便性状改变及体质量减轻等症状，但实验组症状偏重。实验组兔处死后大体标本见肝门部粘连严重，胆总管横断以上扩张，4只出现胆道壁坏死，6只出现肝外带的胆汁潴留性肝脓肿，所有实验动物均可见胆道铸型的存在。对照组兔大体标本见肝内外胆道全部扩张，肝门部无明显粘连，肝内外胆道壁光整，无胆道铸型。病理切片损伤后24h出现肝内大胆管黏膜的大片坏死、脱落；72h可见肝内外大小胆管内均充盈着大量粉染物质，部分大胆管正常腺上皮为扁平上皮覆盖，管壁周围有大量炎细胞浸润；术后21d见大胆管失去正常黏膜上皮，为纤维组织及扁平上皮覆盖。结论胆道铸型综合征动物模型已初步建立，该征起因于胆道上皮的严重损伤，继而出现的炎性反应是胆道铸型形成及出现相关病征的基础。

Objective To establish an animal model for biliary cast syndrome （BCS） of human and investigate the pathological mechanism for BCS. Methods Forty Japanese large-ear rabbits were divided into two groups at random. Biliary endepidermis was damaged with carbolic acid in experiment group rabbits, then a support tube was placed at the breakpoint of bile common duct in each experimental animal. Only support tube was placed at the breakpoint of bile common duct in control group. After four weeks, rabbits were executed, and the liver was dissected for pathological analysis. Results All experiment animals were operated successfully. Six rabbits died at 3rd week after operation. And all animals appeared as listlessness, poor appetite, changes in stool description and loss of weight. The symptoms of experimental group were obviously severe than in control group. There were adhesions at hepatic hilum and distensions at biliary tracts above intersect of common duct in experimental group, 4 rabbits appeared necrosis on biliary tract paries and bile retention hepatapostema in 6 experimental animals. Biliary cast was found in each experimental rabbit liver. There were mild adhesions at hepatic hilum, distensions at biliary tracts above intersect of common duct in control group. The biliary tract paries was slick, and no biliary cast was found in control animal liver. After the damage by carbolic acid, there were biliary endepidermis necrosis and defluvium defluxion in large bile duct at 24th h after operation. There were plenty of pink materials in liver exterior and interior biliary tract at 72nd h after operation. The biliary tract paries was infiltrated by white blood cells and part of biliary endepidermis was placed by flat epithelium. The biliary endepidermis was placed by fibrous tissue and fiat epithelium in large bile duct at 21st day after operation. Conclusion The animal model for BCS has been established successfully. BCS is contributed to the serious damage of biliary endepidermis. The formation of biliary cast and appearance of correlated symptoms are based on the sequentia inflammatory reaction.