title: Effect of nutritional status on oxidative stress in an ex vivo perfused rat liver.
abstract: BACKGROUND
  Normothermic ischemia-reperfusion is a determinant in liver injury occurring during surgical procedures, ischemic state, and multiple organ failure. The preexisting nutritional status of the liver might contribute to the extent of tissue injury and primary nonfunction. The aim of this study was to determine the role of starvation on hepatic ischemia-reperfusion injury in normal rat livers.
  
  
  METHODS
  Rats were randomly divided into two groups: one had free access to food, the other was fasted for 16 h. The portal vein was cannulated, and the liver was removed and perfused in a closed ex vivo system. Two modes of perfusion were applied in each series of rats, fed and fasting. In the ischemia-reperfusion mode, the experiment consisted of perfusion for 15 min, warm ischemia for 60 min, and reperfusion during 60 min. In the nonischemia mode, perfusion was maintained during the 135-min study period. Five rats were included in each experimental condition, yielding a total of 20 rats. Liver enzymes, potassium, glucose, lactate, free radicals, i.e., dienes and trienes, and cytochrome c were analyzed in perfusate samples. The proportion of glycogen in hepatocytes was determined in tissue biopsies.
  
  
  RESULTS
  Transaminases, lactate dehydrogenase, potassium, and free radical concentrations were systematically higher in fasting rats in both conditions, with and without ischemia. Cytochrome c was higher after reperfusion in the fasting rats. Glucose and lactate concentrations were greater in the fed group. The glycogen content decreased in both groups during the experiment but was markedly lower in the fasting rats.
  
  
  CONCLUSIONS
  In fed rats, liver injury was moderate, whereas hepatocytes integrity was notably impaired both after continuous perfusion and warm ischemia in fasting animals. Reduced glycogen store in hepatocytes may explain reduced tolerance.
authors.affiliation: Department of Anesthesiology and Laboratory of Experimental Medicine (ULB 222 Unit), University Hospital Center, Charleroi, Belgium. michael.stadler@chu-charleroi.be
authors.forename: Michaela
authors.initials: M
authors.lastname: Stadler
authors.forename: Vincent
authors.initials: V
authors.lastname: Nuyens
authors.forename: Laurence
authors.initials: L
authors.lastname: Seidel
authors.forename: Adelin
authors.initials: A
authors.lastname: Albert
authors.forename: Jean G
authors.initials: JG
authors.lastname: Boogaerts
mesh_terms: D000818:Animals; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers; D001786:Blood Glucose / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004798:Enzymes / Q000097:blood; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006498:Hepatectomy; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000473:pathology / Q000502:physiology*; D008111:Liver Function Tests; D008112:Liver Glycogen / Q000378:metabolism; D009752:Nutritional Status; D018384:Oxidative Stress / Q000502:physiology*; D010477:Perfusion; D011188:Potassium / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D004798:Enzymes; D008112:Liver Glycogen; D019344:Lactic Acid; D006003:Glycogen; D045304:Cytochromes c; D001663:Bilirubin; D011188:Potassium