par Tosenberger, Alen 
;Ataullakhanov, F;Bessonov, N;Panteleev, M;Tokarev, A;Volpert, Vitaly
Référence Journal of theoretical biology, 337, page (30-41)
Publication Publié, 2013
;Ataullakhanov, F;Bessonov, N;Panteleev, M;Tokarev, A;Volpert, VitalyRéférence Journal of theoretical biology, 337, page (30-41)
Publication Publié, 2013
Article révisé par les pairs
| Résumé : | Hemostatic plug covering the injury site (or a thrombus in the pathological case) is formed due to the complex interaction of aggregating platelets with biochemical reactions in plasma that participate in blood coagulation. The mechanisms that control clot growth and which lead to growth arrest are not yet completely understood. We model them with numerical simulations based on a hybrid DPD-PDE model. Dissipative particle dynamics (DPD) is used to model plasma flow with platelets while fibrin concentration is described by a simplified reaction-diffusion-advection equation. The model takes into account consecutive stages of clot growth. First, a platelet is weakly connected to the clot and after some time this connection becomes stronger due to other surface receptors involved in platelet adhesion. At the same time, the fibrin mesh is formed inside the clot. This becomes possible because flow does not penetrate the clot and cannot wash out the reactants participating in blood coagulation. Platelets covered by the fibrin mesh cannot attach new platelets. Modelling shows that the growth of a hemostatic plug can stop as a result of its exterior part being removed by the flow thus exposing its non-adhesive core to the flow. |
