![]() We previously showed that sickle cell patients with high blood viscosity usually have more frequent vaso-occlusive crises than those with low blood viscosity. In this context, any increase in blood viscosity can promote vaso-occlusive like events. However, in sickle cell disease (SCD) vascular function is impaired. This is the case in healthy individuals when vascular function is intact and able to adapt to blood rheological strains. Indeed, any increase in blood viscosity should promote vasodilation. However, blood viscosity, through its effects on wall shear stress, is a key modulator of nitric oxide (NO) production by the endothelial NO-synthase. Poiseuille’s Law predicts that any increase in blood viscosity should cause a rise in vascular resistance. Indeed, any changes in one or several of these parameters may affect blood viscosity differently. Blood flow in the microcirculation is highly dependent on the ability of RBC to deform, but RBC deformability also affects blood flow in the macrocirculation since a loss of deformability causes a rise in blood viscosity. RBC aggregation occurs at low shear rates, and increases blood viscosity and depends on both cellular (RBC aggregability) and plasma factors. The shear thinning property of blood is mainly attributed to red blood cell (RBC) rheological properties. Both hematocrit and plasma viscosity influence blood viscosity. Blood viscosity is an important determinant of local flow characteristics, which exhibits shear thinning behavior: it decreases exponentially with increasing shear rates. ![]()
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