(545g) A Collision Model of Red Blood Cell Aggregates in Shear Flow

Platelet activation and homotypic aggregation induced by high shear stress or by chemical agonists (e.g., ADP,collagen, or thrombin) are involved in atherosclerosis and accompanying thrombosis cell aggregation and disaggregation in a linear shear flow. A collision model of shear induced cell aggregation and disaggregation is governed by receptor–ligand binding Erythrocyte or Red Blood Cells form aggregates in rouleaux formation with macromolecules (fibrinogen or dextran) present in plasma. Platelet aggregation is one of the first physiological reactions to vessel wall injury. Platelet aggregation at sites of vascular injury is central to the arrest of bleeding and for subsequent vascular repair; however, an exaggerated platelet aggregation response at sites of atherosclerotic plaque rupture can lead to the development of vascular occlusive thrombi, precipitating diseases such as the acute coronary syndromes and is chemic stroke A few seconds after injury, the damaged site is covered with a plug of aggregated platelets. For this process to occur efficiently, platelets must be delivered to the vessel wall and collide with either the damaged site or previously adhered platelets. The lateral migration of cells in flowing blood has been the subject of extensive experiments. Experimental studies indicate that lateral platelet movement is caused by continuous rebounding collisions between erythrocytes. These net collisions produce shear-induced diffusion (dispersion), which locally mixes the plasma and platelets near erythrocytes.

Aggregation is large at low shear rates and as shear rates increase aggregates break up. Bridging model and depletion model are used to analyze thrombus, clot formation. The adhesion of erythrocytes to each other and of erythrocyte to platelets can take place. In the bridging model, it is assumed that fibrinogen or dextran molecules non-specifically adsorb onto the cell membrane and form a ”bridge” to the adjacent cell. In contrast, the depletion model proposes the opposite. In this model, aggregation occurs because the concentration of macromolecules near a RBC surfaces in close proximity is depleted compared to the concentration of the bulk phase, resulting in a net ”depletion” force. RBC aggregation depends on their elastic properties. A model is proposed which considers collisions of platelet with another platelet or with an erythrocyte. Factors such as sizes of the platelets and erythrocyte, concentration of erythrocyte, shear rates in the platelet to platelet adhesion and platelet to erythrocyte adhesion are discussed and compared with available experimental results.