title: Intermittent ischemia enhances the uptake of indocyanine green to livers subject to ischemia and reperfusion.
abstract: OBJECTIVE
  Intermittent ischemia is known to promote post perfusion bile flow, and hence recovery of liver function following ischemia reperfusion of the liver. However, the mechanisms involved are not well understood. The aim of this study was to identify the step(s) in the bile acid transport pathway altered by intermittent ischemia.
  
  
  METHODS
  Arat model of segmental hepatic ischemia in which the bilateral median and left lateral lobes were made ischemic by clamping the blood vessels was used. Indocyanine green (ICG), infrared spectroscopy, and compartmental kinetic analysis, were used to indirectly monitor the movement of bile acids across hepatocytes in situ. Rates of bile flow were measured gravimetrically.
  
  
  RESULTS
  In control livers (not subjected to ischemia), the movement of ICG from the blood to bile fluid could be described by a three compartment model comprising the blood, a rapidly-exchangeable compartment, and the hepatocyte cytoplasmic space. In livers subjected to continuous clamping, the rates of ICG uptake to the liver, and outflow from the liver, were greatly reduced compared with those in control livers. Intermittent clamping (three episodes of 15 min clamping) compared with continuous clamping substantially increased the rate of ICG uptake from the blood but had less effect on the rate of ICG outflow from hepatocytes.
  
  
  CONCLUSIONS
  It is concluded that intermittent ischemia promotes post reperfusion bile flow in the early phase of ischemia reperfusion injury principally by enhancing the movement of bile acids from the blood to hepatocytes.
authors.affiliation: Department of Medical Biochemistry, Flinders University, Adelaide, South Australia, Australia.|The HPB and Liver Transplant Unit, Flinders Medical Centre, and School of Medicine, Flinders University, Adelaide, South Australia, Australia.
authors.forename: Mathilde
authors.initials: M
authors.lastname: Steenks
authors.affiliation: Department of Medical Biochemistry, Flinders University, Adelaide, South Australia, Australia.|The HPB and Liver Transplant Unit, Flinders Medical Centre, and School of Medicine, Flinders University, Adelaide, South Australia, Australia.
authors.forename: Jeroen
authors.initials: J
authors.lastname: Peters
authors.affiliation: Department of Medical Biochemistry, Flinders University, Adelaide, South Australia, Australia.|The HPB and Liver Transplant Unit, Flinders Medical Centre, and School of Medicine, Flinders University, Adelaide, South Australia, Australia.
authors.forename: Willem
authors.initials: W
authors.lastname: Rademacher
authors.affiliation: Department of Surgery, University Medical Centre, Groningen, The Netherlands.
authors.forename: Vincent B
authors.initials: VB
authors.lastname: Nieuwenhuijs
authors.affiliation: The HPB and Liver Transplant Unit, Flinders Medical Centre, and School of Medicine, Flinders University, Adelaide, South Australia, Australia.
authors.forename: Robert T A
authors.initials: RT
authors.lastname: Padbury
authors.affiliation: Department of Medical Biochemistry, Flinders University, Adelaide, South Australia, Australia.
authors.forename: Greg J
authors.initials: GJ
authors.lastname: Barritt
mesh_terms: D000818:Animals; D001646:Bile / Q000378:metabolism; D001647:Bile Acids and Salts / Q000378:metabolism*; D022781:Hepatocytes / Q000378:metabolism; D007208:Indocyanine Green / Q000378:metabolism*; D007511:Ischemia / Q000378:metabolism*; D019194:Ischemic Preconditioning; D008099:Liver / Q000098:blood supply* / Q000378:metabolism*; D008297:Male; D008954:Models, Biological; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D001647:Bile Acids and Salts; D007208:Indocyanine Green