title: Cold preservation of fatty liver grafts: prevention of functional and ultrastructural impairments by venous oxygen persufflation.
abstract: OBJECTIVE
  The incidence of steatosis in livers retrieved for organ transplantation is up to 30%. Due to the shortage of donor organs, many of these livers are accepted for clinical transplantation, although a high rate of graft dysfunction is associated with ischemic preservation of steatotic livers. The present study was intended to reduce the ischemia/reperfusion injury of steatotic grafts by the use of venous systemic oxygen persufflation during cold storage.
  
  
  METHODS
  A histologically-documented mild to moderate steatosis was induced in livers of Wistar rats by fasting for 2 days and subsequent feeding of a fat-free diet enriched in carbohydrates. Fatty livers were retrieved and flushed via the portal vein with 60 ml of HTK. In group A, livers were then stored ischemically at 4 degrees C for 24 h. Livers of group B were additionally connected to a gaseous oxygen supply and persufflated with O2 via the venous vascular system during the cold storage period. Viability of the livers was then assessed upon isolated perfusion in vitro with oxygenated Krebs-Henseleit buffer.
  
  
  RESULTS
  Venous systemic oxygen sufflation resulted in a relevant and significant reduction of parenchymal (ALT: 132+/-90 vs 434+/-172 U/l; p<0.01) and mitochondrial (GLDH: 116+/-57 vs 633+/-241 U/l; p<0.001) enzyme release during reperfusion. Moreover, Kupffer cell activation, as evaluated from acid phosphatase activity in the perfusate, was reduced to about 1/3 (4.0+/-1.3 vs 11.9+/-5.3 U/l; p<0.01). Electron microscopic analysis revealed that the liver mitochondria and sinusoidal endothelial lining were better preserved after oxygen persufflation, which was in line with the data on enzyme release and the increased portal perfusion pressure in the untreated group, while normal values were found after venous systemic oxygen sufflation.
  
  
  CONCLUSIONS
  Venous oxygen persufflation may thus represent a useful tool for the safe and improved preservation of ischemia-sensitive steatotic livers.
authors.affiliation: Division of Surgical Research, Clinic of Surgery, University of Bonn and Institute of Pathology, University of Bonn, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Minor
authors.forename: S
authors.initials: S
authors.lastname: Akbar
authors.forename: R
authors.initials: R
authors.lastname: Tolba
authors.forename: F
authors.initials: F
authors.lastname: Dombrowski
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D015925:Cryopreservation / Q000379:methods*; D005234:Fatty Liver / Q000378:metabolism* / Q000473:pathology; D007728:Kupffer Cells / Q000187:drug effects / Q000648:ultrastructure; D008099:Liver / Q000098:blood supply* / Q000473:pathology; D016031:Liver Transplantation; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects / Q000201:enzymology / Q000648:ultrastructure; D009926:Organ Preservation / Q000379:methods*; D010100:Oxygen / Q000494:pharmacology*; D010477:Perfusion; D011169:Portal Vein / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D014690:Venous Pressure / Q000187:drug effects
chemical_list: D000135:Acid Phosphatase; D010100:Oxygen