title: Oxidative stress in fulminant hepatic failure: comparison of two pig models with and without liver necrosis.
abstract: OBJECTIVE
  No experimental study has clearly demonstrated how liver necrosis worsens the evolution of fulminant hepatic failure. Considering that several types of liver injury are associated with oxidative stress, we decided to measure plasma oxidative markers in two pig models of fulminant hepatic failure without and with liver necrosis.
  
  
  METHODS
  Fulminant hepatic failure was produced in two groups of six pigs each by either total hepatectomy or complete hepatic devascularization. The following parameters were recorded before and during the course of hepatic failure: electrocerebral activity, plasma vitamin E, malondialdehyde and fluorescent protein-aldehyde adducts, total cholesterol, lactate-dehydrogenase, creatine phosphokinase, and ammonium.
  
  
  RESULTS
  Despite comparable survival periods, hepatic necrosis was associated with earlier electrocerebral deterioration. Plasma concentration of malondialdehyde and fluorescent protein-aldehyde adducts rose and vitamin E content decreased in both groups. However, while in the group without liver necrosis the rates of cholesterol and vitamin E decay were identical, in the group with liver necrosis cholesterol concentration decreased less than vitamin E concentration, strongly indicating a true intravascular oxidation of vitamin E. Interestingly, in both models the rise of oxidative parameters preceded the development of cell injury.
  
  
  CONCLUSIONS
  Oxidative stress, although present in both models, was significantly higher in the group with liver necrosis.
authors.affiliation: Istituto di Fisiologia Clinica, CNR, Via Savi, 8-56127 Pisa, Italy. kusmic@ifc.cnr.pi.it
authors.forename: C
authors.initials: C
authors.lastname: Kusmic
authors.forename: U
authors.initials: U
authors.lastname: Boggi
authors.forename: R
authors.initials: R
authors.lastname: Bellini
authors.forename: F
authors.initials: F
authors.lastname: Vistoli
authors.forename: M
authors.initials: M
authors.lastname: Castellari
authors.forename: G
authors.initials: G
authors.lastname: Taddei
authors.forename: A
authors.initials: A
authors.lastname: Minervini
authors.forename: F
authors.initials: F
authors.lastname: Filipponi
authors.forename: F
authors.initials: F
authors.lastname: Mosca
authors.forename: R
authors.initials: R
authors.lastname: Barsacchi
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D018736:DNA Adducts / Q000097:blood; D004195:Disease Models, Animal; D004569:Electroencephalography; D006501:Hepatic Encephalopathy / Q000503:physiopathology*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000503:physiopathology; D008106:Liver Cirrhosis, Experimental / Q000503:physiopathology*; D008111:Liver Function Tests; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology*; D000644:Quaternary Ammonium Compounds / Q000097:blood; D013552:Swine; D014810:Vitamin E / Q000097:blood
chemical_list: D018736:DNA Adducts; D000644:Quaternary Ammonium Compounds; D014810:Vitamin E; D008315:Malondialdehyde; D002784:Cholesterol; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase