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Arterial thrombi consist mainly of platelets and fibrin, the biopolymer produced in the final step of the coagulation cascade. Thrombus fragmentation may result in occlusion of smaller distal vessels (embolization), a serious and often fatal event. The objective of this study is to investigate the role of the fibrin polymer network on the resistance of a clot to fragmentation under shear flow. For that purpose, a fibrin clot model representative of native clots is submitted to a shear flow that reproduces the pathophysiological range of shear stress. The adhesion force due to specific fibrin/fibrin interactions is determined from the measurement of the shear stress producing 50% detachment of model particles of blood platelets embedded in the clot. This force was found to be several orders higher than the nonspecific colloidal forces between surfaces, which can, thus, be neglected. Influence of the number of fibrin monolayers in the clot model on adhesion force is investigated.
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Lorthois et al. (2000) studied this question.
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