title: Portosystemic collaterals are not prerequisites for the development of hepatic encephalopathy in cirrhotic rats.
abstract: BACKGROUND
  Liver functions and portosystemic collaterals influence the development and severity of hepatic encephalopathy (HE) in cirrhosis. However, it has not been examined which factor has a greater influence or if shunts can be used to determine the presence and severity of HE. The expression of tumor necrosis factor-α (TNF-α) is increased in cirrhosis, and its role in HE deserves further evaluation.
  
  
  METHODS
  Portal hypertension was induced by portal vein ligation (PVL; a model of high-degree portosystemic shunting without significant liver damage) and liver cirrhosis was induced by bile duct ligation (BDL; a model of low-degree shunting with liver cirrhosis) in male Spraque-Dawley rats. Sham-operated rats were used as controls. Motor activity counts, hemodynamic parameters, plasma levels, liver biochemistry parameters, TNF-α, and a flow-pressure curve study of portosystemic collaterals (where a higher slope indicates fewer portosystemic collaterals) were performed on Day 7 after PVL and Week 5 after BDL.
  
  
  RESULTS
  Portal pressure was significantly higher in the PVL and BDL groups than in controls. The liver biochemistry parameters, TNF-α, and motor activities were not significantly different between the PVL and PVL-control groups. In the BDL group, TNF-α, AST, and total bilirubin levels were significantly higher and the motor activity counts were lower than in the BDL-control group. Moreover, in the BDL rats, TNF-α (p=0.037, R=-0.490), AST (p=0.007, R=-0.595) and total bilirubin (P=0.001, R=-0.692) levels, but not the slopes of the flow-pressure curves, were significantly and negatively correlated with the motor activity counts.
  
  
  CONCLUSIONS
  The presence of a high degree of portosystemic shunting without significant liver damage may not be adequate for the development of HE.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC.
authors.forename: I-Fang
authors.initials: IF
authors.lastname: Hsin
authors.forename: Sun-Sang
authors.initials: SS
authors.lastname: Wang
authors.forename: Hui-Chun
authors.initials: HC
authors.lastname: Huang
authors.forename: Fa-Yauh
authors.initials: FY
authors.lastname: Lee
authors.forename: Cho-Yu
authors.initials: CY
authors.lastname: Chan
authors.forename: Ching-Chih
authors.initials: CC
authors.lastname: Chang
authors.forename: Chia-Yang
authors.initials: CY
authors.lastname: Hsu
authors.forename: Han-Chieh
authors.initials: HC
authors.lastname: Lin
authors.forename: Shou-Dong
authors.initials: SD
authors.lastname: Lee
mesh_terms: D000818:Animals; D003097:Collateral Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D006439:Hemodynamics; D006501:Hepatic Encephalopathy / Q000209:etiology*; D006975:Hypertension, Portal / Q000503:physiopathology*; D008106:Liver Cirrhosis, Experimental / Q000150:complications*; D008297:Male; D009043:Motor Activity; D011168:Portal System / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D014409:Tumor Necrosis Factor-alpha