title: [Preserving remnant liver function after major hepatic vein occlusion].
abstract: OBJECTIVE
  To observe the pathological changes of the remained hepatic lobe after major hepatic vein (MHV) occlusion.
  
  
  METHODS
  Seventy-eight rats were randomly divided into the control group, the ligation group of segmental hepatic vein, the stricture group of left MHV, and the ligation group of left MHV. The pathology, hepatic microcirculation and hemodynamic changes of the involved hepatic lobe of MHV occlusion were dynamically determined.
  
  
  RESULTS
  Necrosis occurred in the hepatocytes at the first postoperative day in the ligation group of MHV. Extensive collaterals between the hepatic veins and the portal veins appeared in the periphery of involved liver lobe in the stricture group of MHV. The levels of endotoxin and TXB(2)/6-Keto-PGF1alpha in the blood of portal vein obviously increased in the ligation group of MHV and also increased in the stricture group of MHV. The levels of endotoxin and TXB(2)/6-Keto-PGF1alpha in the blood of portal vein in the ligation and stricture group of MHV were apparently higher than those in the ligation group of segmental hepatic vein and in the control group.
  
  
  CONCLUSIONS
  The involved liver tissue can not tolerate complete MHV occlusion. The hepatic tissue lacking of MHV drain not only loss its function, but also cause endotoxemia and disorder of hepatic microcirculation. The involved hepatic lobe after the MHV ligation should have been resected at the same time.
authors.affiliation: Institute of Organ Transplantation, Tongji Medical University, Wuhan 430030.
authors.forename: X
authors.initials: X
authors.lastname: Xing
authors.forename: S
authors.initials: S
authors.lastname: Xia
authors.forename: H
authors.initials: H
authors.lastname: Guo
authors.forename: H
authors.initials: H
authors.lastname: Deng
authors.forename: S
authors.initials: S
authors.lastname: Ma
authors.forename: L
authors.initials: L
authors.lastname: Zuo
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D004731:Endotoxins / Q000097:blood; D006503:Hepatic Veins / Q000503:physiopathology / Q000601:surgery; D006504:Hepatic Veno-Occlusive Disease / Q000209:etiology / Q000503:physiopathology*; D008026:Ligation / Q000009:adverse effects; D008099:Liver / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D008102:Liver Circulation; D008297:Male; D009336:Necrosis; D011169:Portal Vein / Q000503:physiopathology / Q000601:surgery; D051381:Rats; D017207:Rats, Sprague-Dawley; D013929:Thromboxane B2 / Q000097:blood; D013997:Time Factors
chemical_list: D004731:Endotoxins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha