The role of thrombin activatable fibrinolysis inhibitor and factor XI in platelet-mediated fibrinolysis resistance: a thromboelastographic study in whole blood.

摘要: Summary. Background: The resistance of platelet-rich thrombi to fibrinolysis is generally attributed clot retraction and platelet PAI-1 release. The role TAFI in platelet-mediated lysis unclear. Objective: We investigated the contribution antifibrinolytic effect platelets whole blood by thromboelastography. Methods: Platelet-poor (PP-WB,  400 × 103 μL−1) samples were obtained from normal human (N-WB, 150–220 × 103 μL−1). Clot time was measured thromboelastography recalcified supplemented with t-PA (100 ng mL−1) tissue factor (1:1000 Recombiplastin). Results: t-PA-induced increased parallel concentration (up 3-fold). Neutralization TAFI, but not PAI-1, shortened ∼ 50% PR-WB < 10% PP-WB. Accordingly, prothrombin F1+2 TAFIa accumulation greater than A similar TAFI-dependent inhibition observed when prevented cytochalasin D or abciximab, membranes tested. Moreover, an intact contact system, attenuated anti-FXI anti F-XII antibody. Finally, made clots resistant profibrinolytic heparin concentrations displaying a strong anticoagulant activity. Conclusions: Our data indicate that activation one major mechanism whereby make underscore importance inhibitors as new antithrombotic agents.