Abstract The hemorrhagic diathesis after transplantation of preserved livers generally is attributed to intravascular coagulation, whereas postoperative “hypercoagulability” of the blood is considered the main cause of thrombosis of the hepatic artery anastomosis. Since our preliminary studies, however, suggested other mechanisms, parameters of coagulation, fibrinolysis, and platelet function were prospectively studied before and after 28 orthotopic liver transplantations, with and without preservation, in dogs and pigs. In addition, the arterial anastomoses were evaluated routinely by angiography and, after removal at reintervention or autopsy, inspected for thrombosis and tested for fibrinolytic activity and fibrin deposition. Concerning the hemorrhagic diathesis, prolongation of bleeding time without concomitant thrombocytopenia was the main abnormality found and occurred only in the nine dogs with liver transplants previously preserved for 3 to 6 hours. As only two of the nine dogs had postoperative hemorrhage of clinical significance, we consider surgically imperfect hemostasis facilitated by an acquired platelet dysfunction the principal cause of hemorrhage. Thrombosis of the arterial anastomosis was found in 38 percent of animals in which an end-to-end anastomosis was made but was not encountered with celiac artery-aorta anastomoses. Local factors due to surgical technique therefore appear most important in the pathogenesis of thrombosis of the hepatic artery anastomosis, although the postoperative hyperfibrinogenemia and diminished local and systemic fibrinolytic activity may contribute as well.