Institut Camille Jordan, UMR 5208 CNRS, University Lyon 1, 69622 Villeurbanne, France; INRIA Team Dracula, INRIA Antenne Lyon la Doua, 69603 Villeurbanne, France.
National Research Center for Haematology, Ministry of Health and Social Development of Russian Federation, Novii Zykovskii pr., 4a, 125167 Moscow, Russia; Federal Research and Clinical Centre of Paediatric Haematology, Oncology and Immunology, Ministry of Health and Social Development of Russian Federation, Samori Marshela str., 1, 117198 Moscow, Russia; Faculty of Physics, M. V. Lomonosov Moscow State University, GSP-1, 1-2 Leninskiye Gory, 119991 Moscow, Russia; Center for Theoretical Problems of Physicochemical Pharmacology, Russian Academy of Sciences, Kosygina str., 4, 119991 Moscow, Russia.
J Theor Biol. 2013 Nov 21;337:30-41. doi: 10.1016/j.jtbi.2013.07.023. Epub 2013 Jul 31.
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.
止血塞覆盖在损伤部位(或病理情况下的血栓)上,是由于聚集的血小板与参与血液凝固的血浆中的生化反应之间的复杂相互作用而形成的。控制血栓生长并导致生长停止的机制尚不完全清楚。我们使用基于混合 DPD-PDE 模型的数值模拟来对其进行建模。耗散粒子动力学(DPD)用于模拟带有血小板的血浆流动,而纤维蛋白浓度则由简化的反应-扩散-对流方程来描述。该模型考虑了血栓生长的连续阶段。首先,血小板与血栓弱连接,一段时间后,由于涉及血小板黏附的其他表面受体,这种连接变得更强。同时,纤维蛋白网在血栓内部形成。这是因为血流不会穿透血栓,并且不能冲洗掉参与血液凝固的反应物。被纤维蛋白网覆盖的血小板无法附着新的血小板。模拟表明,止血塞的生长可能会停止,因为其外部部分被流动移除,从而使未附着的核心暴露于流动中。