Rj. Porte et al., ROLE OF THE DONOR LIVER IN THE ORIGIN OF PLATELET DISORDERS AND HYPERFIBRINOLYSIS IN LIVER-TRANSPLANTATION, Journal of hepatology, 21(4), 1994, pp. 592-600
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.