Normal intravascular blood clotting (hemostasis) and its pathological
counterpart, thrombosis, occur under flow and this can profoundly
influence the progress of clot formation. This talk will focus on two
different aspects of our efforts to model and probe the interactions
of flow and clotting. One involves the biochemistry of the
coagulation enzyme network and how the behavior of this system is
affected by flow-mediated platelet deposition on an injury and by
flow-mediated transport of the enzymes and their precursors. The
other involves a continuum model that describes platelet thrombosis
initiated by a ruptured atherosclerotic plaque in a
coronary-artery-sized vessel. This model includes full treatment of
the fluid dynamics, and the aggregation of platelets in response to
the plaque rupture and further chemical signals. Among the behaviors
seen with this model are the growth of wall-adherent platelet thrombi
to occlude the vessel and stop the flow, and the transient growth and
subsequent embolization of thrombi leaving behind a passivated injured
surface.