Abstract
We have found that glycoprotein IIb:IIIa (GPIIb:IIIa) expressed on nonstimulated platelets is the primary receptor for platelet adhesion to immobilized fibrinogen or fibrin. At low shear rates of the blood the interaction between GPIIb:IIIa and fibrin(ogen) is strong enough to resist the shear forces exerted on the platelet as was shown with experiments with antibodies against platelet membrane glycoproteins and perfusion studies with blood from patients lacking platelet membrane receptors. Impaired platelet adhesion to fibrin(ogen) was found with blood from a patient with Glanzmann's thrombasthenia (lacking GPIIb:IIIa), blood from patients with the Bernard-Soulier syndrome (lacking GPIb) and blood from patients with severe von Willebrand's disease. This indicates that at higher shear rates additional interactions via GPIb on the platelet and von Willebrand factor originating from plasma or platelets are necessary to increase the affinity of the platelet for fibrin(ogen).
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