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 annexin V 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 annexinV 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.
Keywords
vWF - SIPA(ct) - flow chamber - cone-plate viscometer - platelet collision