title: Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation.
abstract: OBJECTIVE
  To determine the relative contribution of the gastrointestinal tract and the liver in lactate metabolism in patients with acute liver failure (ALF) and the effect of liver transplantation on this. We hypothesized that the liver and gut are net producers of lactate in ALF and that this is reversed after liver transplantation.
  
  
  METHODS
  A university-affiliated specialist liver transplant operating theater.
  
  
  METHODS
  Eleven patients with ALF undergoing liver transplantation.
  
  
  METHODS
  After ethical approval, 11 patients with ALF listed for orthotopic hepatic transplantation were studied. Whole blood was analyzed for lactate concentration from radial artery (RA) catheter, portal vein (PV), and hepatic vein (HV) during the dissection phase and was repeated postreperfusion of the liver graft. Gradients across the gut and the liver were calculated to see if there was net production or consumption.
  
  
  RESULTS
  HV lactate was significantly higher than arterial (p =.028) in patients with ALF before liver transplantation, suggesting splanchnic production of lactate. Total splanchnic lactate gradient (HV-RA) is positive in ALF. Both the gut (PV-RA) and the liver (HV-PV) were net producers of lactate. After liver transplantation, hepatic venous lactate falls below arterial levels but not significantly. The gradient across the gut (PV-RA) remained positive, but the transhepatic gradient (HV-PV) became significantly negative, showing consumption by the graft (p =.021). The magnitude of lactate consumption after transplantation correlated positively with portal venous lactate concentration (p =.029) and inversely with graft cold ischemic time (p =.007).
  
  
  CONCLUSIONS
  The liver is a net producer of lactate in patients with ALF and an elevated whole blood lactate. After liver transplantation, the graft becomes a consumer of lactate as shown by the negative lactate gradient. The degree of consumption is dependent on portal venous lactate concentration and cold ischemic time.
authors.affiliation: Institute of Liver Studies, Kings College Hospital, London, UK.
authors.forename: N D
authors.initials: ND
authors.lastname: Murphy
authors.forename: S K
authors.initials: SK
authors.lastname: Kodakat
authors.forename: J A
authors.initials: JA
authors.lastname: Wendon
authors.forename: C A
authors.initials: CA
authors.lastname: Jooste
authors.forename: P
authors.initials: P
authors.lastname: Muiesan
authors.forename: M
authors.initials: M
authors.lastname: Rela
authors.forename: N D
authors.initials: ND
authors.lastname: Heaton
mesh_terms: D005260:Female; D006503:Hepatic Veins; D006801:Humans; D019934:International Normalized Ratio; D007413:Intestinal Mucosa / Q000378:metabolism*; D019344:Lactic Acid / Q000096:biosynthesis / Q000097:blood*; D017114:Liver Failure, Acute / Q000209:etiology / Q000378:metabolism*; D016031:Liver Transplantation; D008297:Male; D011169:Portal Vein; D011184:Postoperative Period; D017534:Radial Artery
chemical_list: D019344:Lactic Acid