Hepatocellular defence against acidosis is preserved after cold storage.
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 degrees 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 microL-1 min-1 and initial Na+/HCO3- symport-mediated HCO3- fluxes 7 +/- 2, 7 +/- 3 and 6 +/- 2 nmol microL-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.


CONCLUSIONS
Altered pHi homeostasis is unlikely to play a role in the pathogenesis of primary non-function of liver allografts.
Department of Clinical Pharmacology, University of Berne, Switzerland.
B
B
Helbling
E L
EL
Renner
D000138:Acidosis; D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D002478:Cells, Cultured; D003080:Cold Temperature; D005978:Glutathione; D006863:Hydrogen-Ion Concentration; D007328:Insulin; D017136:Ion Transport; D016014:Linear Models; D008099:Liver / Q000166:cytology*; D016031:Liver Transplantation; D008297:Male; D009926:Organ Preservation; D019188:Organ Preservation Solutions; D011887:Raffinose; D051381:Rats; D017207:Rats, Sprague-Dawley
D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose