title: Role of neutrophils in sinusoidal endothelial cell injury after extensive hepatectomy in cholestatic rats.
abstract: OBJECTIVE
  The authors have shown previously that sinusoidal endothelial cell injury developed concomitantly with the accumulation of neutrophils in the hepatic sinusoidal space in cholestatic rats after extensive hepatectomy. The aim of the present study was to investigate the role of neutrophils in the development of this kind of endothelial cell injury.
  
  
  METHODS
  Rats underwent 78% partial hepatectomy after 2 weeks of cholestasis, and subsequent external biliary drainage for 5 days. To decrease the number of neutrophils, antirat neutrophil serum was administered intraperitoneally. Some serum parameters and histological specimens were examined 48 h after partial hepatectomy.
  
  
  RESULTS
  Anti-neutrophil serum significantly reduced the number of accumulated neutrophils in the hepatic sinusoids. Although the purine nucleoside phosphorylase: alanine aminotransferase ratio, a marker of non-parenchymal cell injury, was increased in cholestatic-hepatectomized rats, this abnormality was significantly attenuated by the treatment with antineutrophil serum. Electron microscopically, focal detachment of cytoplasms of sinusoidal endothelial cells was observed occasionally in cholestatic-hepatectomized rats, but was not found in the antirat neutrophil serum-treated rats.
  
  
  CONCLUSIONS
  These results indicate that accumulated neutrophils might be important effector cells in the pathogenesis of sinusoidal endothelial cell injury after extensive hepatectomy in cholestatic rats, even after appropriate external biliary drainage.
authors.affiliation: First Department of Surgery, School of Medicine, Chiba University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohtsuka
authors.forename: M
authors.initials: M
authors.lastname: Miyazaki
authors.forename: H
authors.initials: H
authors.lastname: Kubosawa
authors.forename: Y
authors.initials: Y
authors.lastname: Kondo
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: H
authors.initials: H
authors.lastname: Shimizu
authors.forename: Y
authors.initials: Y
authors.lastname: Shimizu
authors.forename: S
authors.initials: S
authors.lastname: Nozawa
authors.forename: S
authors.initials: S
authors.lastname: Furuya
authors.forename: N
authors.initials: N
authors.lastname: Nakajima
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D002630:Chemotactic Factors / Q000378:metabolism; D002779:Cholestasis / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D004727:Endothelium / Q000201:enzymology / Q000473:pathology; D006133:Growth Substances / Q000378:metabolism; D006498:Hepatectomy / Q000009:adverse effects*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D018375:Neutrophil Activation / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology*; D011683:Purine-Nucleoside Phosphorylase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric; D015996:Survival Rate
chemical_list: D002630:Chemotactic Factors; D006133:Growth Substances; D018799:Intercellular Adhesion Molecule-1; D011683:Purine-Nucleoside Phosphorylase; D000410:Alanine Transaminase