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Modeling the mechanics of blood clotting

Special Events

Speaker: Robert Guy, University of Utah
Location: 1147 MSB
Start time: Mon, Jan 30 2006, 4:10PM

Damage to a blood vessel wall initiates both platelet aggregation and fibrin gel formation. Platelets attach to collagen, and tissue factor initiates coagulation, which involves a tightly regulated network of enzyme reactions. The final product of these reactions is the enzyme thrombin, which acts as a chemical signal to activate platelets allowing them to stick together. Thrombin also converts the plasma protein fibrinogen into fibrin monomer, that polymerizes to form fibrin gel.

To explore the formation of fibrin gel, simple models of flow, coagulation, and gelation are combined to explore how the shear rate and other parameters control the formation of fibrin gel. A different framework is used to model platelet aggregation in large arteries. The blood and aggregating platelets are treated as a single fluid with varying material properties to account for links between platelets. There are two distinct spatial scales, the scale of the fluid and the much smaller scale of platelet--platelet interactions. Activated platelets interact to form elastic links on the smaller scale. These links influence the fluid flow by the addition of an extra stress. The presence of two spatial scales makes the problem extremely difficult to analyze or to simulate. An approximation that closes the system on the fluid scale is presented. The closure model is compared with the multiscale model using asymptotic analysis for steady shear flow and numerical simulations for more complicated flows. Computational results are presented in different vessel geometries that model the partial occlusion of the vessel due to atherosclerosis. These simulations demonstrate the profound role fluid dynamics and clot mechanics might play in the development of blood clots.