中文摘要：

目的 探讨犬肝移植中肝动脉不同的灌注方式造成的缺血／再灌注损伤对术后多药耐药相关蛋白2（MRP2）的表达和胆红素代谢的影响。方法 取20只犬建立简易原位自体肝移植模型。将模型犬随机分为4组，每组5只。对照组：术中不进行灌注，维持麻醉及剖腹状态；肝动脉缺血组（HAI组）：经胃十二指肠动、静脉插管进行肝脏冷灌注，肝下下腔静脉切口作为流出道，灌注20min后依次开放肝上、肝下下腔静脉及门静脉，缝合下腔静脉切口，肝动脉持续阻断2h后开放；门静脉和肝动脉同时灌注组（SR组）：于开放门静脉的同时，开放肝动脉，灌注方法同HAI组；肝动脉桥式转流组（HABS组）：在冷灌注前先解剖脾动脉、插管，并将脾动脉插管与胃十二指肠动脉插管以三通接头相连，建立桥式通道。灌注完毕开放门静脉的同时开放桥式通道，肝动脉持续阻断2h后开放，并关闭桥式通道。检测各组再灌注后0、2、4和8h时肝细胞MRP2的积分吸光度A值及胆汁内胆红素含量。结果 在0h时，各组MRP2的吸光度A值及胆汁内胆红素含量的差异均无统计学意义（P〉0．05）；以0h为基点，HAI组MRP2的吸光度A值和胆汁内胆红素含量在4h时分别下降了52．6％和23．1％，SR组下降了39．8％和11．8％，HABS组下降了44．2％和14．4％。同一时点间各组的检测结果比较，差异均有统计学意义（P〈0．01）。MRP2的表达和胆汁内胆红素含量之间呈正相关（r=0．699，P=0．001）。结论 肝移植中肝动脉桥式转流的灌注方式操作较简便，对移植肝的损伤程度较轻。缺血／再灌注损伤可引起MRP2表达抑制，而MRP2表达下降可能是导致高胆红素血症的机制之一。

英文摘要：

Objective To investigate the impact of expression of MRP2 and metabolism of bilirubin resulting by hepatic ischemia reperfusion injury （HIRI） and the difference of three kinds of reperfusion styles, and to provide objective evidence for founding new pathway to prevent or relieve the hyperbilirubinemia after liver transplantation. Methods Orthotopic liver transplantation modes were established in 20 dogs. The animals were randomly divided into into control group, SR group, HAI group and HABS group according to cold reperfusion or not and different styles of reperfusion. The expression of MRP2 and the level of biliary bilirubin were detected. Results At 0 h, the integral optical density （IOD） of hepatocellular MRP2 and level of biliary bilirubin had no significant difference between control and test groups （P〉0. 05）. As compared with control group, the IOD value of MRP2 and level of bilirubin in 3 test groups were decreased significantly at 2 h, 4 h and 8 h （P〈0.01）, most markedly in HAI group. At 4 h, the IOD of MRP2 and level of biliary bilirubin were descended by 52. 6% and 23. 1%, 44. 2% and 14. 4%, 39. 8% and 11.8% in HAI group, HABS group and SR group, respectively. Conclusions HIRI can markedly inhibit the expression and function of hepatocellular MRP2 in liver transplantation, which probably it is an important mechanism that causes cholestasis and hyperbilirubinemia after liver transplantation. Persistent HAI can aggravate inhibition of the expression of MRP2 and disorder of bilirubinic metabolism. HABS can lessen inhibition of MRP2 and preclude or relieve the disorder of bilirubinic metabolism.