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Effects of von Willebrand factor concentration and platelet collision on shear-induced platelet activation.

The binding of plasma von Willebrand factor (vWF) to platelet glycoprotein (GP) Ibalpha 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 microg/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 microg/ml to 25 microg/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.