In the control group, a significant decrease in platelet aggregability could be demonstrated after reperfusion. This was paralleled by a decrease in platelet counts. When PGE1 was infused during OLT, the post-reperfusional decreases in platelet aggregability and platelet counts in the control group could be prevented. Furthermore, our investigation demonstrated that PGE1 infusion led to higher t-PA activity during the anhepatic phase. This was paralleled and followed by lower alpha 2AP levels at the end of the anhepatic phase and after reperfusion. The higher t-PA levels in the PG group did not result in clinical signs of hyperfibrinolysis during OLT. The aprotinin administration in both groups is most certainly responsible for the absence of hyperfibrinolytic signs in the TEG and the low overall requirement for transfusions, explaining the comparable transfusion rate in the two groups (Fig. 5). Further investigations involving more patients are required to evaluate the clinical effect of PGE1 therapy.