An independent haemostatic mechanism: shear induced platelet aggregation

Advances in Experimental Medicine and Biology
J R O'Brien, G P Salmon

Abstract

We have published (1) evidence indicating that high shearing forces alone applied to platelets expose and activate a unique domain on glycoprotein IIb/IIIa (GPIIb/IIIa) at the platelet surface. In the presence of von Willebrand's factor (vWf) and divalent cations the platelets will aggregate. This paper reviews the extensive literature on high shear effects. It describes a device in which high shear produced by forcing heparinised whole blood through a complex filter normally results in platelet activation; the platelets aggregate and then block the filter. This system is inhibited by antibodies to GPIIb/IIIa and to vWf: fibrinogen is apparently not involved. The same antibodies to GPIIb/IIIa and vWf prevent high shear induced thrombosis occurring in vivo in animal models. The filter blockage is not influenced by aspirin, heparin and ticlopidine and so involves a different mechanism from the aspirin sensitive mechanisms involved in clinical thrombosis prevention in vivo in man. While there are a number of unexplained phenomena in this global test nevertheless this filter model is a simple way of studying a recently recognised pathway which is almost certainly involved in thrombogenesis in man.

Citations

Jan 27, 1998·Circulation·B S Coller
Feb 5, 2010·Annals of Biomedical Engineering·D BluesteinK B Manning
Nov 9, 2017·ASAIO Journal : a Peer-reviewed Journal of the American Society for Artificial Internal Organs·Zengsheng ChenZhongjun J Wu

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