Thermic transition and glycolytic capacity as critical events in the survival of rat liver slices after overnight cold hypoxic preservation.

Cellular survival and hypoxia-reoxygenation injury in overnight cold-preserved liver slices (+/-20 h at 4 degrees C) were investigated. Increased cell death after overnight cold hypoxia depended more on temperature than on the reoxygenation process itself. Fructose (at 50 mM) added before the onset of hypoxia improved survival at the end of 20 h of cold hypoxia over Krebs- or glucose-treated slices. Such a protective effect by fructose was also seen during the normothermic (37 degrees C) reoxygenation of previously cold hypoxic-preserved slices, but only in the absence and not in the presence of tert-butyl hydroperoxide, a model compound widely used to induce an oxidative stress. The protection by fructose was equivalent to that observed when liver slices were incubated in the University of Wisconsin solution (UW). Finally, the morphological study of haematoxylin and eosin (H & E)-stained slices has shown cytoplasmic vacuoles during the reoxygenation step, which were more pronounced in UW-treated than in fructose-treated slices.