Summary

The binding of plasma von Willebrand factor (vWF) to platelet glycoprotein (GP) Ibα in a high shear stress field,and subsequent integrin-GPIIb/IIIa-vWF conjunction induces platelet aggregation (SIPA).However,the specific biomechanical mechanism of the vWF-GPIb interaction still remains to be elucidated.A parallel- plate rectangular flow chamber was built to simulate a stenopeic artery flow pattern. Using the flow chamber, we examined shear-induced platelet activation (SIPAct) at different vWF concentrations (5–25 μg/ml) and several simulated stenotic high shear rates. P-selectin expression on the platelets and annexinV binding to the platelets were used as two markers of platelet activation. At different localized shear rates (3,000 s-1–9,500 s-1), the percentage of annexin V and P-selectin positive cells increased from 8.3 ± 0.4% to 22.3 ± 1.8% ( p 0.05) and from 17.4 ± 0.5% to 33.5 ± 2.5% (p 0.05), respectively.As the vWF concentration increased from 5 μg/ml to 25 μg/ml, the annexin V binding rate increased from 7.2 ± 0.6% to 53.4 ± 3.8% (p 0.05), and P-selectin expression increased from 16.5 ± 1.2% to 65.9 ± 5.2% (p 0.05). A test in a uniform shear field using cone-plate viscometer rheometry showed that the platelet activation rate was proportional to the platelet concentration.This result suggests that platelet collision is one of the impact factors of SIPAct.