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Intracellular Na+ accumulation and hepatocyte injury during cold storage
R Carini1, M G De Cesaris, G Bellomo
1Department of Medical Sciences, University of East Piedmont A. Avogadro, Novara, Italy.
Background:
The mechanisms responsible for liver damage during cold storage are still not completely understood. We have investigated the role played by alterations of Na+ homeostasis in cell injury during cold hypoxia.
Methods:
The changes in Na+ distribution were investigated in isolated rat hepatocytes stored at 4 degrees C under hypoxic conditions.
Results:
Hepatocyte cold stored up to 72 hr in Krebs-Henseleit-Hepes buffer showed a progressive increase in intracellular Na+ content that preceded the loss of cell viability. Na+ accumulation and cell death were prevented using Na+-free, acidic (pH 6.5) or glycine-supplemented storage media. The Na+ ionophore monensin reverted the cytoprotection exerted by glycine and by the acidic medium, but not that given by Na+-free Krebs-Henseleit-Hepes. A low Na+ content was also important for the cytoprotection observed using University of Wisconsin solution.
Conclusions:
Na+ overload might contribute to liver graft injury occurring during cold storage.