On the coagulation of platelet-rich plasma - Physiological mechanism and pharmacological consequences

Thrombin formation and blood platelet reactions are intimately linked in ha emostasis and in thrombosis. In vivo, procoagulant phospholipids required f or the coagulation mechanism are mainly provided by activated platelets, an d thrombin is the most potent platelet activator. To study these interactio ns, an ancient tool of coagulation physiology, the thrombin generation test , was revived and the results obtained were reviewed. The amount of thrombi n activity that develops, expressed as the endogenous thrombin potential (t he area under the thrombin generation curve), is influenced by the clotting factors (except XII and XIII), the activated protein C system and natural inhibitors on the one hand and by platelet activity on the other. The plate let reactions that we found to be involved are induced by thrombin via glyc oprotein (GP) Ilb/IIIa activation and by fibrin via interaction with GPIb. von Willebrand factor is crucial in both reactions and therefore an obligat ory factor for normal thrombin generation in the presence of platelets. All antithrombotics, be it anticoagulants (e.g. OAC, all heparins or hirudin) or antiplatelet drugs (aspirin, GPIIb/IIIa blockers) diminish thrombin gene ration.