ULTRASTRUCTURE OF HUMAN LIVER GRAFTS PRESERVED WITH UW SOLUTION - COMPARISON BETWEEN PATIENTS WITH LOW AND HIGH POSTOPERATIVE TRANSAMINASESLEVELS

We studied the morphology of sinusoidal cells on 21 human liver grafts prior to harvesting, at the end of the preservation period in UW solu tion, and after complete revascularization. The mean cold ischemic per iod was 11 h 34 min. Immediate follow-up was uneventful in 20 of these cases; 13 showed a mean peak of postoperative transaminases below 1,3 00 IU/L (group A), and 7 above 1,500 IU/L (group B). In the case of on e patient (group C) steatosis was severe (50%) and there was serious p ostoperative dysfunction (transaminases 18,000 IU/L). Biopsies were pe rfusion-fixed by the transparenchymal route to ensure satisfactory ult rastructural results. In group A, some sinusoidal endothelial cells pr esented signs of activation at the end of the preservation period, and even more after revascularization. Kupffer cells also presented signs of activation particularly after reperfusion. Signs of endothelial ce ll damage with gaps and partial rupture of the plasmic membrane mere a lso observed, particularly after revascularization in areas which cont ained numerous inflammatory cells adhering to the wall. The sinusoidal pole of hepatocytes was occasionally damaged, with the formation of b lebs. In group B, adhesion of inflammatory cells to the sinusoidal wal l was increased. Furthermore, in some areas with endothelial cell dama ge, neutrophils and platelets infiltrated the Disse space, and hepatoc ytes were increasingly damaged. In the case of patient C, the most obv ious signs after reperfusion were hepatocyte drop out and death but th ere was no evidence of any concomitant sinusoidal cell damage. It woul d appear that even in cases where immediate follow-up is eventful, end othelial and Kupffer cells show signs of activation. This can be assoc iated with signs of microcirculatory disturbances as was seen in 4 cas es in group B. In the only case of severe steatosis that we studied, t he essential sign was death of hepatocytes.