Cold ischemia-reperfusion injury of the liver. Role of the liver donor nutritional status in rats.

To verify the role of donor nutritional status on the quality of liver preservation after cold storage, we assessed hepatocyte and liver endothelial cell viabilities and functions in an isolated perfused rat liver model. Livers from fed and fasted Wistar rats were isolated and perfused either immediately after liver harvesting or after a 24-hr cold (4 degrees C) preservation in University of Wisconsin solution. Hyaluronic acid (150 ng/ml) and taurocholate (11.5 micrograms/ml) were infused into the reservoir, and their eliminations were assessed to evaluate liver endothelial cell function and hepatocyte function, respectively. Liver viability was estimated by intrahepatic resistance, oxygen consumption, bile secretion, and lactate dehydrogenase release. In addition, cell viabilities were evaluated by trypan blue staining. In fed-rat livers, glycogen content did not differ before or after the cold preservation, although a reduction was observed during the subsequent perfusion period. Liver glycogen content in fed rats was markedly higher than in the fasted rats at each time point studied. In fasted and fed rats, liver viability parameters and hepatocyte function were moderately altered, whereas liver endothelial cell function was markedly impaired after cold preservation. However, feeding had no influence on either hepatocyte or liver endothelial cell functions which were similarly altered in both nutritional conditions. The present data show that the nutritional status of liver donors does not play an important role in the preservation of liver endothelial cells after cold ischemia-reperfusion and, thus, should not affect the overall resistance of livers to hypothermic-ischemic injury.