title: Partial liver ischemia is followed by metabolic changes in the normally perfused part of the liver during reperfusion.
abstract: BACKGROUND
  Temporary vascular in- and outflow occlusion is an effective technique for bleeding control during liver resection. However, occlusion can result in ischemia/reperfusion (I/R) injury to the liver. The aim of this study in a porcine model was to investigate the effect of in- and outflow occlusion of part of the liver on the metabolism of the normally perfused parenchyma of the same liver measured by microdialysis.
  
  
  METHODS
  Eight pigs underwent laparotomy. A microdialysis catheter was inserted into in the left and right part of the liver, respectively. Microdialysis samples were collected every 30 min. Occlusion of the left part of the liver was achieved for 60 min, followed by 5 h of reperfusion. Samples were analyzed for glucose, lactate, pyruvate and glycerol. Blood samples were drawn to determine standard liver and biochemical parameters.
  
  
  RESULTS
  Comparing the ischemic part of the liver with the normally perfused part, significant differences in the levels of lactate, pyruvate and glycerol were found. During reperfusion, similar and continuous decreases below baseline levels were observed for lactate and pyruvate in both the ischemic and normally perfused part of the liver. No significant changes in liver parameters or blood glucose levels were seen.
  
  
  CONCLUSIONS
  Partial ischemia of the liver is without effects on metabolism in the normally perfused part. Metabolic changes in the ischemic part of the liver were reversible. However, partial liver ischemia was followed by similar continuous decreases in lactate and pyruvate levels in the whole liver, even though the ischemic insult was not detectable in transaminase levels.
authors.affiliation: Department of Surgical Gastroenterology L, Aarhus University Hospital, Aarhus, Denmark. askannerup @ gmail.com
authors.forename: A-S
authors.initials: AS
authors.lastname: Kannerup
authors.forename: H
authors.initials: H
authors.lastname: Grønbæk
authors.forename: P
authors.initials: P
authors.lastname: Funch-Jensen
authors.forename: S
authors.initials: S
authors.lastname: Karlsen
authors.forename: F V
authors.initials: FV
authors.lastname: Mortensen
mesh_terms: D000818:Animals; D015179:Colorectal Neoplasms; D004195:Disease Models, Animal; D005260:Female; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D007511:Ischemia / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism; D008099:Liver / Q000098:blood supply* / Q000293:injuries / Q000378:metabolism* / Q000601:surgery; D008113:Liver Neoplasms / Q000098:blood supply / Q000556:secondary / Q000601:surgery; D017551:Microdialysis; D019289:Pyruvic Acid / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism*; D034421:Sus scrofa
chemical_list: D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol