ABSTRACT
Liver transplantation has become a well-accepted treatment modality for end-stage liver diseases, but the procedure can be associated with bleeding complications influencing perioperative mortality and morbidity. The clearly elevated levels of neopterin and cathepsin B in the graft liver perfusate, resulting in increases immediately after graft reperfusion, are suggestive of ischemic damage or activation of the graft liver macrophages/monocytes with release after revascularization. The role of mediators released from leukocytes in hyperfibrinolysis during orthotopic liver transplantation (OLT) is speculative. The increase in plasminogen activator inhibitor observed after revascularization of the graft in OLT by blocking systemic plasmin generation may be important for the development of a disseminated intravascular coagulation -like situation. Thrombin generation is stimulated by activated leukocytes in several ways. Tissue factor expression on macrophages/monocytes after different “direct” stimuli as well as cytokine-mediated is a long-known phenomenon.
