Shear-induced platelet activation and platelet microparticle formation in native human blood

• Published in: Thrombosis research Vol. 92; no. 6; pp. S33 - S41
• Main Authors: Sakariassen, Kjell S., Holme, Pl A., Ørvim, Una, Marius Barstad, R., Solum, Nils O., Brosstad, Frank R.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 15.12.1998
• Subjects: Adult; Blood Platelets - physiology; Blood Platelets - ultrastructure; Cytoplasmic Granules - physiology; Cytoplasmic Granules - ultrastructure; FITC; fluorescein isothiocyanate; Humans; Mab; Male; Microparticle formation; monoclonal antibody; Platelet Activation; Platelet Glycoprotein GPIIb-IIIa Complex - physiology; Shear; Shear activation; Stress, Mechanical; Thrombus formation; von Willebr and factor; vWF; Thrombus formation; FITC; Shear; vWF; Shear activation; Microparticle formation; Mab
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/S0049-3848(98)00158-3

Shear-induced platelet activation and platelet microparticle formation are triggered in native human blood by high arterial shear or by a sudden increase in shear as introduced by a stenosis with potential consequences for collagen-induced platelet thrombus formation. Blood was drawn from healthy volunteers and directly perfused ex vivo over various well-defined eccentric stenoses. Shear-induced platelet activation was determined by using flow cytometry to assess: 1) GPIIb-IIIa activation by fluorescein isothiocyanate (FITC)-labeled Mab PAC-1; and 2) translocation of membrane aminophospholipids (procoagulant activity) by FITC-labeled Annexin V. Microparticle formation was measured by flow cytometry and FITC-labeled Mab Y2/51 directed against GPIIIa. Significant platelet activation and platelet microparticle formation were elicited when the wall shear rate reached 10,500 sec −1 for a period of 0.075 sec. Prolonged exposure to or a rapid increase in shear further enhanced activation and microparticle formation. Shear-induced platelet activation was associated with significantly increased collagen-induced platelet thrombus formation that was insensitive to aspirin ingestion. Exposure of native blood to very high shear thus activates platelets to express GPIIb-IIIa, renders the platelet membrane procoagulant and stimulates microparticle formation. These responses are associated with enhanced collagen-induced thrombus formation by prostaglandin-independent mechanisms.