Effect of fibrinolytic agents on platelet thrombus formation in an in vitro perfusion system

Previous study has shown that, at blood flow rate corresponding to high wall shear rates, thrombosis is regulated by the concentration and molecular weight distribution of von Willebrand factor (vWF). vWF binding to GP Ib mediates platelet interaction with subendothelium (adhesion). vWF, together with plasma proteins, supports platelet interactions with those platelets already adherent (aggregation). By using an in vitro model that mimics blood flow inside an injured vessel, this paper investigates the effect of fibrinolytic agents on cellular/molecular hemostatic mechanisms. As a result, image processing shows both a decrease in platelet adhesion and in subsequent aggregation. There is no difference in platelet accumulation at low wall shear rates. Pharmacologic concentrations of streptokinase SK cause degradation of platelet GP Ib in PRP.