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Exposure of platelets to shear stress leads to aggregation in the absence of exogenous agonists. We have now found that different adhesive proteins and platelet membrane glycoproteins are involved in aggregation depending on the shear stress condi- tions and the concentration of divalent cations in the medium. When blood is collected with trisodium citrate as anticoagu- lant, which causes a decrease in the levels of external ionized calcium (ICa2+I), platelet aggregation can be induced under low shear force (12 dyn/cm2) and is mediated by fibrinogen binding to the glycoprotein Hib-Mila complex. Aggregates formed under these conditions are not stable, and when shear force is in- creased to 68 dyn/cm2, disaggregation results. By contrast, platelets from blood collected with hirudin as anticoagulant, wherein ICa2+10 is within normal plasma levels, do not undergo low shear-induced aggregation; however, after exposure to a shear force above 80 dyn/cm2, aggregation is observed but only when von Willebrand factor is present and can interact with both its platelet binding sites, glycoprotein Ib-IX and glycopro- tein Jib-Mia. Fibrinogen is not involved in high shear-induced aggregation which, in fact, occurs normally in patients with severe afibrinogenemia. Thus, von Willebrand factor in the ab- sence of exogenous agonists can mediate platelet aggregation in experimental conditions that may mimic the hemorheological situation of partially occluded arteries. This pathway of platelet aggregation involving only one adhesive ligand and two mem- brane adhesion receptors may play a relevant role in thrombo- genesis. (
Ikeda et al. (Mon,) studied this question.