Premium
Hepatocellular defence against acidosis is preserved after cold storage
Author(s) -
Helbling,
Renner
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00303.x
Subject(s) - antiporter , intracellular , intracellular ph , viaspan , pathogenesis , acidosis , chemistry , homeostasis , hepatocyte , biochemistry , endocrinology , medicine , transplantation , membrane , in vitro
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 + /HCO 3 − symport‐mediated HCO 3 − 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 pH i homeostasis is unlikely to play a role in the pathogenesis of primary non‐function of liver allografts.