Recombinant factor VIIa enhances platelet adhesion and activation under flow conditions at normal and reduced platelet count.

摘要: Summary. Background: Recombinant factor VIIa (rFVIIa), which was developed for treatment of inhibitor-complicated hemophilia, appears suitable as prohemostatic agent in other clinical disorders including patients with thrombocytopenia. It is generally accepted that rFVIIa functions by enhancement thrombin generation at the site injury. is, however, unknown if and how this affects platelet adhesion aggregation. Objectives: To determine effect rFVIIa-mediated on aggregation under flow conditions normal reduced counts. Methods: Washed platelets red cells were combined to obtain plasma-free blood different The reconstituted perfused over a collagen- or fibrinogen-coated surface absence presence generating system consisting purified coagulation factors rFVIIa, (F)X prothrombin. Results: Addition FX prothrombin washed enhanced collagen spreading fibrinogen count numbers low 10 000 µL−1. activation state measured intracellular calcium fluxes, exposure procoagulant phospholipids annexin A5 binding. Conclusions: Taken together, increased formation may explain therapeutic effects thrombocytopenic (i) primary hemostasis (ii) leading elevated fibrin formation.