<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>The occurrence of biliary stricutures in allografts following liver transplantation correlates
with the duration of preservation time. The correlation between preservation time
and biliary strictures suggests that anoxic or reperfusion injury of the bile duct epithelium
causes stricture formation. However, the relative susceptibility of bile duct cells to anoxic
or reoxygenation injury is unknown. Our aims were to determine the vulnerability of rat
liver bile duct cells to anoxic and reoxygenation injury and to compare the results with
hepatocytes. During anoxia, bile duct epithelial cells were significantly more resistant to
cell killing than hepatocytes. Rates of cellular proteolysis were also 2.5-fold lower in bile
duct cells than in hepatocytes during anoxia. In contrast to anoxia, reoxygenation of
anoxic cells increased cell killing of bile duct cells but improved viability of hepatocytes.
The rate of toxic oxygen species formation by bile duct cells was 5-fold greater than in
hepatocytes during reoxygenation. In addition, basal levels of glutathione are lower in bile
duct cells than in hepatocytes. These data suggests that bile duct cells are more susceptible
to reoxygenation injury than to anoxia. These studies support the hypothesis that
reoxygenation injury during liver preservation leads to bile duct injury during liver
transplantation.</p>
[]
HPB Surg. 1996; 9(2):113-115