Abstract:
The formation of a clot is an exquisitely regulated biological process in which a complex fluid, blood, undergoes a rapid transformation into a densely packed porous medium at the site of a vascular injury. This talk will focus on how mass transfer regulates blood clot initiation and growth. At the site of an injury, proteins found in the vascular wall initiate a set of biochemical reactions collectively called coagulation. At early times (~10 min), the ability to form a stable clot depends on the flux coagulation products from the wall compared to their dilution by transport mechanisms. I will examine this problem in the context of hemophilia, which is a bleeding disorder that results in diminished flux of the enzyme thrombin. At longer times (~10-60 min), blood clots assemble into a heterogeneous porous medium. I will show evidence that hindered solute transport into and out of clots is a biophysical mechanism that works in concert with biochemical inhibitors to arrest clot growth.