Metabolism of hyaluronic acid by liver endothelial cells: effect of ischemia-reperfusion in the isolated perfused rat liver.

Liver endothelial cells appear to be particularly vulnerable to cold ischemia reperfusion. However, their function has not yet been evaluated, except using electron microscopic changes and trypan blue exclusion (an index of cell death). Hyaluronic acid is a polysaccharide highly extracted by normal liver endothelial cells. We thus evaluated liver endothelial cell function by measuring hyaluronic acid elimination in a model of ischemia-reperfusion injury using isolated perfused Wistar rat livers. We compared the effects of two preservation solutions during cold ischemia (4 degrees C): normal saline with 2 mM CaCl2 (4 h and 8 h ischemia) and the University of Wisconsin solution (8 h and 24 h ischemia). Eliminations were measured during two 40-min periods before and after ischemia; during each period, hyaluronic acid (150 ng/ml) and also, to evaluate hepatocyte function, propranolol (100 ng/ml) were infused into the reservoir. We show that, whatever the preservation solution or time used, liver endothelial cell function is altered to a larger extent than hepatocyte function. University of Wisconsin solution does not appear to protect liver endothelial cells during preservation, particularly after 24 h of cold ischemia. Hyaluronic acid elimination can be a useful tool in the investigation of an ideal preservation solution to protect liver endothelial cells from ischemia-reperfusion damage.