title: Oxygen consumption, lactate metabolism, and gastric intramucosal pH in an experimental liver transplantation model.
abstract: OBJECTIVE
  To assess the usefulness of measuring whole-body oxygen consumption (VO2), arterial lactate concentration, and gastric intramucosal pH (pHi) as parameters for evaluating hepatic graft viability in a model of experimental liver transplantation.
  
  
  METHODS
  Experimental, prospective study.
  
  
  METHODS
  Hospital laboratory for experimental surgery.
  
  
  METHODS
  Twenty-eight Landrace-Largewhite pigs: 14 donors and 14 recipients.
  
  
  METHODS
  Orthotopic liver transplantation. Two groups were differentiated by graft preservation status: an optimal-graft group (group 1), which received donor livers that had been preserved in Collins solution at 4 degrees C for <4 hrs (n = 7), and an injured-graft group (group 2), which received donor livers that had been preserved in Collins solution at 4 degrees C for >24 hrs (n = 7).
  
  
  RESULTS
  Hemodynamic parameters, variables related with systemic and hepatic oxygen and lactate metabolism, gastric pHi, and arterial pH were measured at two stages: a) preanhepatic stage; and b) neohepatic stage (60 mins after reperfusion). There were no differences in VO2 between graft groups or stages. In the neohepatic stage, hepatic oxygen extraction and lactate turnover were significantly higher in the optimal-graft group than in the injured-graft group. In the neohepatic stage, gastric pHi decreased significantly and arterial lactate concentrations increased significantly in both groups.
  
  
  CONCLUSIONS
  Changes in hepatic VO2 cannot be detected by VO2 measurements. Optimal-state grafts increased their lactate turnover as a result of substrate overload, but injured grafts did not. Therefore, the evolution of arterial lactate concentrations in the immediate postoperative period may be useful for the early evaluation of transplanted livers. Gastric pHi can be a useful measurement in the immediate posttransplantation period for differentiating between hyperlactacidemia produced by liver dysfunction (normal pHi) and hyperlactacidemia produced by lactate generation as a consequence of inadequate tissue oxygenation or of a mixed origin (abnormal pHi).
authors.affiliation: Pediatric Intensive Care Unit, Hospital Infantil La Paz, Madrid, Spain.
authors.forename: J I
authors.initials: JI
authors.lastname: Muñoz-Bonet
authors.forename: M
authors.initials: M
authors.lastname: López-Santamaria
authors.forename: F
authors.initials: F
authors.lastname: Ruza-Tarrio
authors.forename: J A
authors.initials: JA
authors.lastname: Paz-Cruz
authors.forename: J
authors.initials: J
authors.lastname: Roque
authors.forename: M
authors.initials: M
authors.lastname: Gamez
authors.forename: C
authors.initials: C
authors.lastname: Grande
authors.forename: J
authors.initials: J
authors.lastname: Murcia
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D005745:Gastric Acidity Determination; D005753:Gastric Mucosa / Q000378:metabolism*; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D016031:Liver Transplantation / Q000379:methods / Q000502:physiology* / Q000706:statistics & numerical data; D010101:Oxygen Consumption; D011446:Prospective Studies; D013552:Swine
chemical_list: D015415:Biomarkers; D019344:Lactic Acid