title: Significance of morphological alteration by portal vein branch ligation in endotoxin-induced liver injury after partial hepatectomy.
abstract: BACKGROUND
  Regenerating liver after partial hepatectomy (PH) is susceptible to endotoxin. This study was conducted to investigate how morphological alteration by preoperative portal vein branch ligation (PVL) affects endotoxin-induced liver injury after PH.
  
  
  METHODS
  Male Sprague-Dawley rats were divided into a PVL group undergoing left PVL and into a non-PVL group receiving a sham operation. Seven days later, animals in both groups were subjected to PH (the left lateral, median and caudate lobes). Lipopolysaccharide (LPS) was intravenously administered to both groups 2 days after PH.
  
  
  RESULTS
  A significant increase in hepatocyte and sinusoidal endothelial cell proliferation assessed by Ki-67 immunostaining reached a peak at day 2 and 3 after PVL, respectively, in accordance with the changes in plasma interleukin-6 concentrations after PVL. The proliferation response of these cells after PH was observed in both groups, showing a significantly weaker response in the PVL group. The sinusoidal width after PH was significantly reduced in the non-PVL group when compared with that in the PVL group. LPS administration induced a marked elevation of plasma tumour necrosis factor-alpha levels in the non-PVL group compared with the PVL group. PVL before PH significantly attenuated endotoxin-induced functional and structural liver damage with greater hepatic polymorphonuclear leucocyte infiltration and microcirculatory derangement, resulting in an improvement in the 7-day survival rate.
  
  
  CONCLUSIONS
  Morphological alteration by PVL is of great advantage in preventing the development of endotoxin-induced liver injury in the regeneration process after PH.
authors.affiliation: Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan. sota@hama-med.ac.jp
authors.forename: Shigeyasu
authors.initials: S
authors.lastname: Ota
authors.forename: Shohachi
authors.initials: S
authors.lastname: Suzuki
authors.forename: Takanori
authors.initials: T
authors.lastname: Sakaguchi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Baba
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mitsuoka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nakamura
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Konno
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001663:Bilirubin / Q000097:blood; D049109:Cell Proliferation; D056486:Chemical and Drug Induced Liver Injury; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000473:pathology; D006498:Hepatectomy / Q000379:methods; D022781:Hepatocytes / Q000473:pathology; D015850:Interleukin-6 / Q000097:blood; D019394:Ki-67 Antigen / Q000032:analysis; D008026:Ligation; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D008107:Liver Diseases / Q000097:blood / Q000473:pathology* / Q000503:physiopathology / Q000517:prevention & control; D008115:Liver Regeneration; D008297:Male; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000473:pathology; D011169:Portal Vein / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D019394:Ki-67 Antigen; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; C433788:lipopolysaccharide, E. coli O26-B6; D001219:Aspartate Aminotransferases; D001663:Bilirubin