ROLE OF THE DONOR LIVER IN THE ORIGIN OF PLATELET DISORDERS AND HYPERFIBRINOLYSIS IN LIVER-TRANSPLANTATION

We investigated the role of the donor liver in the origin of platelet disorders and hemostatic defects in liver transplantation. Eighteen pi gs received an orthotopic or a heterotopic, auxiliary liver graft. Liv er biopsies were taken for electron microscopic studies 5-10 min after reperfusion in nine animals. Blood samples were taken from the first hepatic outflow and from the systemic circulation before and 5 min aft er graft recirculation. Electron microscopy did not show any evidence of microthrombi or platelet aggregation in the graft, either after ort hotopic liver transplantation or after heterotopic liver transplantati on. Most blood platelets, which were lying free in the sinusoids, show ed cell processes and many seemed to have lost their granulae, suggest ing a degree of platelet activation. There were also signs of phagocyt osis of platelets by the Kupffer cells. In the hepatic outflow, platel et count was significantly lower (p<0.05) and fibrinolytic activity si gnificantly higher (p<0.01), than systemic post-reperfusion values. Th ere were no important changes in the coagulation parameters. No signif icant changes were found between the effects on hemostasis of orthotop ic and auxiliary graft reperfusion. In the second part of the study ev idence for platelet activation was found after graft reperfusion in hu man liver transplantation. Plasma levels of platelet factor-4 and beta -thromboglobulin increased significantly after graft reperfusion. Thes e studies suggest that platelet disorders and increased fibrinolytic a ctivity are the major components of the hemostatic defect after graft recirculation in liver transplantation. Sequestration of platelets in the graft is probably due to the accumulation of (activated and degran ulated) platelets in the sinusoids and phagocytosis by Kupffer cells. (C) Journal of Hepatology.