Intracellular Na+ accumulation and hepatocyte injury during cold storage

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 Nat content that preceded t he loss of cell viability. Na+ accumulation and cell death were prevented u sing Na+-free, acidic (pH 6.5) or glycine-supplemented storage media. The N a+ 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 U niversity of Wischonsin solution. Conclusions. Na+ overload might contribute to liver graft injury occurring during cold storage.