Model of the role of transport on agonist distribution and thrombus architecture. As platelets within a developing thrombus become activated, they change shape, retract, and pack tightly together driving the formation of the LTR. This leads to the retention of larger agonists, such as thrombin, within the LTR. Smaller agonists, such as ADP and TxA2, are able to diffuse more freely out of the LTR. The localization of these agonist gradients drives continued platelet activation in the LTR leading to core formation consisting of high platelet packing density, decreased solute transport, α-granule exocytosis, and fibrin deposition. The restriction of thrombin to the core contributes to the shell consisting of loosely adherent platelets, high solute transport, reduced platelet activation, and no fibrin.
