RESUMO
Objective To investigate the protective effect of peroxisome proliferator receptor γcoactivator (PGC)-1αon he-patic ischemia-reperfusion injury .Methods The rat model of hepatic ischemia-reperfusion injury was established .The expression of PGC-1αwas detected by Western blot after 12 hours of reperfusion .The changes of reactive oxygen species(ROS) ,ATP level and serum liver enzyme activity were measured ,and the liver function was evaluated .On the other hand ,PGC-1α lentiviral overexpres-sion vector was constructed and transfected in rat before ischemia-reperfusion .After ischemia-reperfusion ,the expression of PGC-1α,liver ROS ,ATP level were measured by Western blot to explore the protective role of PGC-1αin liver ischemia reperfusion inju-ry .Results The expression of PGC-1α in ischemia-reperfusion liver was significantly lower than that in the control group (P<0 .05) .The level of ROS[(325 .4 ± 70 .9)RLU vs .(108 .5 ± 25 .2)RLU ,P<0 .05] ,the ALT activity in serum [(367 .8 ± 82 .7)U/L vs .(98 .7 ± 16 .8 )U/L ,P<0 .05]in ischemia-reperfusion liver were increased than that in the control group ,whereas liver ATP production was reduced[(6 .1 ± 3 .7)pmol vs .(19 .8 ± 3 .1)pmol ,P<0 .05)] .The expression of PGC-1αin the liver was significantly up-regulated by PGC-1αlentiviral overexpression vector (57 .3 ± 21 .3) U/L vs .(311 .2 ± 25 .8) U/L ,P<0 .05) ,down-regulated ROS[(98 .7 ± 18 .9)RLU vs .(300 .2 ± 45 .6)RLU ,P< 0 .05] and serum glutamic-pyruvic transaminase[(105 .3 ± 21 .3)U/L vs . (311 .2 ± 25 .8)U/L ,P<0 .05)] ,and increased liver ATP production [(17 .3 ± 3 .1)pmol vs .(5 .8 ± 2 .0)pmol ,P<0 .05]in contrast to non-transfected rats .Conclusion PGC-1αcontributes to protect liver ischemia reperfusion injury .
RESUMO
Cold perfusion of liver can significantly alleviate the ischemia-reperfusion injury caused by hepatic blood flow occlusion. We have modified the technique of cold perfusion of liver and applied it to total pancreatectomy for patients with pancreatic head carcinoma complicated with metastasis to the body and tail of pancreas and with portal invasion. After skeletonization of the hepatoduodenal ligament, the amputation of the portal vein and blockage of the superior mesentoric vein were performed before portal perfusion. Meanwhile, pancreatic head resection, duodenectomy, subtotal gastrectomy and partial resection of the superior mesenteric vein and portal vein were carried out. Superior mesenteric vein and portal vein bypass grafting was achieved with artificial vessels. The digestive tract was reconstructed after it was freed of the spleen and resection of the body and tail of pancreas to the left side of superior mesenteric vein, greater omentum and intestine from the end of the colon to splenic flexure of colon. The patient was followed up for 3 months, and the general condition was good, although diarrhea frequently occurred. No tumor metastasis occurred.