Oxygen consumption, lactate metabolism, and gastric intramucosal pH in an experimental liver transplantation model.

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.

DESIGN

Experimental, prospective study.

SETTING

Hospital laboratory for experimental surgery.

SUBJECTS

Twenty-eight Landrace-Largewhite pigs: 14 donors and 14 recipients.

INTERVENTIONS

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).

MEASUREMENTS AND MAIN 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).