Hepatocellular defence against acidosis is preserved after cold storage

• Published in: European journal of clinical investigation Vol. 28; no. 6; pp. 456 - 465
• Main Authors: HELBLING, B, RENNER, E. L
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01.06.1998; Blackwell; Blackwell Publishing Ltd
• Subjects: Acidosis; Adenosine; Allopurinol; Animals; Biological and medical sciences; Cells, Cultured; Cold Temperature; Glutathione; Hepatocyte; Hydrogen-Ion Concentration; Insulin; intracellular pH; Ion Transport; Linear Models; Liver - cytology; liver Na+/H+ antiport; Liver Transplantation; Liver, biliary tract, pancreas, portal circulation, spleen; Male; Medical sciences; Na+/HCO3− symport; Organ Preservation; Organ Preservation Solutions; primary graft non-function; Raffinose; rat; Rats; Rats, Sprague-Dawley; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the digestive system; transplantation; University of Wisconsin solution; Cell function; Rat; Pathogenesis; Liver; Rodentia; Ion transport; Hepatic disease; Transplantation; Experimental study; Homotransplantation; Graft failure; Vertebrata; Mammalia; Organ preservation; Hepatocyte; Surgery; Animal; pH; Digestive diseases
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1046/j.1365-2362.1998.00303.x

Background Primary non‐function of liver allografts is related to preservation time, during which hypoxia leads to intracellular accumulation of acid. Preservation‐induced failure of hepatocellular pH regulation may play a role in the pathogenesis of primary graft non‐function. Methods Using cultured/suspended rat hepatocytes and fluorimetric determination of intracellular pH, we determined whether preservation in University of Wisconsin solution (4°C) impairs hepatocellular defence mechanisms against acidosis. Results In non‐preserved, 24‐h‐preserved and 48‐h‐preserved hepatocytes acidified to pH 6.7–6.8, initial Na+/H+ antiport‐mediated H+ fluxes averaged 12 ± 5, 9 ± 5 and 12 ± 5 nmol μL−1 min−1 and initial Na+/HCO3− symport‐mediated HCO3− fluxes 7 ± 2, 7 ± 3 and 6 ± 2 nmol μL−1 min respectively (P = NS). Preservation did not affect the inverse relationship between Na+/H+ antiport activity and intracellular pH. Thus, hepatocellular defence against intracellular acidosis is maintained during up to 48 h in University of Wisconsin solution. Conclusion Altered pHi homeostasis is unlikely to play a role in the pathogenesis of primary non‐function of liver allografts.