Significance of morphological alteration by portal vein branch ligation in endotoxin-induced liver injury after partial hepatectomy.
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.
Ota
Shigeyasu
S
Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan. sota@hama-med.ac.jp
Suzuki
Shohachi
S
Sakaguchi
Takanori
T
Baba
Satoshi
S
Mitsuoka
Hiroshi
H
Nakamura
Satoshi
S
Konno
Hiroyuki
H
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
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