An independent haemostatic mechanism: shear induced platelet aggregation.
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.
O'Brien
J R
JR
Central Laboratory, St. Mary's Hospital, Portsmouth, Hants., UK.
Salmon
G P
GP
D004912:Erythrocytes / Q000502:physiology; D006487:Hemostasis; D006801:Humans; D008954:Models, Biological; D010974:Platelet Aggregation; D010980:Platelet Membrane Glycoproteins / Q000502:physiology*; D013314:Stress, Mechanical; D013927:Thrombosis / Q000097:blood
D010980:Platelet Membrane Glycoproteins