Significance of morphological alteration by portal vein branch ligation in endotoxin-induced liver injury after partial hepatectomy

Liver Int. 2007 Oct;27(8):1076-85. doi: 10.1111/j.1478-3231.2007.01552.x.

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.

MeSH terms

  • Animals
  • Aspartate Aminotransferases / blood
  • Bilirubin / blood
  • Cell Proliferation
  • Chemical and Drug Induced Liver Injury
  • Disease Models, Animal
  • Endothelial Cells / pathology
  • Hepatectomy* / methods
  • Hepatocytes / pathology
  • Interleukin-6 / blood
  • Ki-67 Antigen / analysis
  • Ligation
  • Lipopolysaccharides
  • Liver / metabolism
  • Liver / pathology*
  • Liver / physiopathology
  • Liver / surgery
  • Liver Diseases / blood
  • Liver Diseases / pathology*
  • Liver Diseases / physiopathology
  • Liver Diseases / prevention & control
  • Liver Regeneration*
  • Male
  • Neutrophil Infiltration
  • Neutrophils / pathology
  • Portal Vein / surgery*
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Interleukin-6
  • Ki-67 Antigen
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • lipopolysaccharide, E. coli O26-B6
  • Aspartate Aminotransferases
  • Bilirubin