title: L-carnitine ameliorates abnormal vulnerability of steatotic rat livers to cold ischemic preservation.
abstract: BACKGROUND
  Up to 30% of all livers retrieved for organ transplantation exhibit steatotic transformations. Chronic organ-donor shortage has led to the acceptance of these organs for transplantation, although a higher risk of graft nonfunction is associated with the preservation of steatotic livers.
  
  
  METHODS
  A dietary steatosis was induced in Wistar rats by fasting them for 2 days and feeding them with a fat-free diet. Fatty livers (n=14) were retrieved and flushed with 60 mL of histidine, tryptophane, alpha-ketoglutarate (HTK) solution. In half of the experiments, L-carnitine (5 mM) was added to the HTK. Functional integrity of the livers was evaluated by isolated reperfusion with KHB in a recirculating system at 37 degrees C for 45 minutes.
  
  
  RESULTS
  Addition of L-carnitine to the HTK promoted a significant reduction of the enzyme leakage from the livers upon reperfusion. Release of alanine-aminotransferase was reduced to one third (127+/-22 vs. 423+/-61 U/L), and the loss of glutamate dehydrogenase in the perfusate could be reduced significantly (42+/-7 vs. 542+/-134 U/L) when compared with livers stored without additional medication. Morphologic corroboration of these data was obtained by electron microscopy. Although normal appearance of liver mitochondria was preserved at the end of the cold ischemic storage, reperfusion of cold-stored fatty livers entailed massive alterations and frequent destruction of hepatic mitochondria. However, these morphologic impairments were remarkably mitigated in the carnitine-treated group.
  
  
  CONCLUSIONS
  L-carnitine represents a feasible metabolic adjunct for a safe and more successful preservation of ischemia-reperfusion-sensitive steatotic livers.
authors.affiliation: Surgical Research Division, Department of Surgery, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany. rtolba@uni-bonn.de
authors.forename: René H
authors.initials: RH
authors.lastname: Tolba
authors.forename: Uwe
authors.initials: U
authors.lastname: Pütz
authors.forename: Dorothee
authors.initials: D
authors.lastname: Decker
authors.forename: Frank
authors.initials: F
authors.lastname: Dombrowski
authors.forename: Holger
authors.initials: H
authors.lastname: Lauschke
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D002331:Carnitine / Q000627:therapeutic use*; D005234:Fatty Liver / Q000473:pathology*; D005947:Glucose / Q000494:pharmacology; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D007511:Ischemia / Q000517:prevention & control*; D008099:Liver / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D009926:Organ Preservation / Q000379:methods; D011189:Potassium Chloride / Q000494:pharmacology; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion
chemical_list: C039984:Bretschneider cardioplegic solution; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D005969:Glutamate Dehydrogenase; D000410:Alanine Transaminase; D005947:Glucose; D002331:Carnitine