Abstract
In the presence of macromolecules, e.g., dextrans, polylysines, heparin, or various plasma proteins, red blood cells (RBCs) aggregate to form rouleaux. Aggregation of RBCs results in an acceleration of erythrocyte sedimentation rate and an elevation of low-shear blood viscosity. The mechanism of RBC aggregation has been postulated to be due to macromolecular bridging between adjacent cell surfaces. The bridging energy is a function of the nature of binding and the number of binding sites between the macromolecules and the cell surfaces. RBC surface is negatively charged due to the presence of sialic acids. The interaction of surface potentials results in a mutual repulsion between cells, especially in the presence of macromolecules. The magnitude of the repulsion is a function of the surface charge density and the ionic composition of the fluid medium. RBC aggregation occurs when the bridging force due to surface adsorption of macromolecules overcomes the electrostatic repulsive force and mechanical shearing force. The net aggregating energy is stored as a change in membrane strain energy. Studies on the ultrastructure of RBC aggregates have shown that the intercellular distance is a function of macromolecular dimensions and that the shape of RBC aggregates is determined by the net aggregating energy. understanding the force balance in RBC interactions serves to establish the physicochemical principles of cell-to-cell interactions induced by macromolecules. It also provides basic information for the understanding of micromechanics of RBC aggregation in blood rheology.
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