Figure 3.
Figure 3. Fibrin-associated multimeric VN potentiates platelet adhesion and aggregation. Whole-blood perfusions were performed for 5 minutes at a shear rate of 500 s–1 on (A) fibrin in the absence or presence of increasing amounts of VN (0 to 143 nM). Platelet coverage shows a VN-dependent increase. A detail of single platelets adherent to fibrin (Ai; B) or fibrin plus VN (Aii; C)(143 nM) is shown (original magnification, × 1000). In a duplicate set of experiments, perfusions were performed on (D) immobilized VN or on clots composed of fibrin or fibrin with 143 nM VN in the absence or presence of control huMab, huMab VN18 directed against multimeric VN, Moab C17 against the βIIIa subunit of the VN-receptor, Poab A0080 against fibrin(ogen), and after preincubation of the fibrin/VN network with PAI-1 (100 μg/mL). Perfusion results are shown as mean coverage (%) ± SEM.

Fibrin-associated multimeric VN potentiates platelet adhesion and aggregation. Whole-blood perfusions were performed for 5 minutes at a shear rate of 500 s–1 on (A) fibrin in the absence or presence of increasing amounts of VN (0 to 143 nM). Platelet coverage shows a VN-dependent increase. A detail of single platelets adherent to fibrin (Ai; B) or fibrin plus VN (Aii; C)(143 nM) is shown (original magnification, × 1000). In a duplicate set of experiments, perfusions were performed on (D) immobilized VN or on clots composed of fibrin or fibrin with 143 nM VN in the absence or presence of control huMab, huMab VN18 directed against multimeric VN, Moab C17 against the βIIIa subunit of the VN-receptor, Poab A0080 against fibrin(ogen), and after preincubation of the fibrin/VN network with PAI-1 (100 μg/mL). Perfusion results are shown as mean coverage (%) ± SEM.

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