Intracellular Na+ accumulation and hepatocyte injury during cold storage

Transplantation. 1999 Jul 27;68(2):294-7. doi: 10.1097/00007890-199907270-00023.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine / pharmacology
  • Allopurinol / pharmacology
  • Analysis of Variance
  • Animals
  • Cell Survival
  • Cold Temperature
  • Cryoprotective Agents / pharmacology
  • Glutathione / pharmacology
  • Insulin / pharmacology
  • Liver / chemistry*
  • Liver / cytology*
  • Male
  • Monensin / pharmacology
  • Organ Preservation / methods*
  • Organ Preservation Solutions / pharmacology
  • Raffinose / pharmacology
  • Rats
  • Rats, Wistar
  • Sodium / metabolism

Substances

  • Cryoprotective Agents
  • Insulin
  • Organ Preservation Solutions
  • University of Wisconsin-lactobionate solution
  • Allopurinol
  • Monensin
  • Sodium
  • Glutathione
  • Adenosine
  • Raffinose