Whole blood is a two-phase liquid, composed of cellular elements suspended in plasma, an aqueous solution containing organic molecules, proteins, and salts ( Baskurt and Meiselman, 2003). Although the role of blood viscosity in vascular adaptations is often ignored, these studies clearly demonstrate that vascular geometry and blood viscosity should not be considered separately when studying the regulation of vascular resistance in healthy populations or in people with cardiovascular diseases. As a result, vascular resistance and arterial pressure increase ( Vazquez et al., 2010 Salazar Vazquez et al., 2011). Therefore, a rise in blood viscosity is not accompanied by an increase in vasodilation. When vascular dysfunction is present, vasodilation is impaired. However, evidence shows that these vascular adaptations can only occur in a functioning vascular system with a healthy endothelium. They also showed that increasing blood viscosity promoted the activation of endothelial NO-synthase through shear stress-dependent mechanisms, resulting in higher NO production, compensatory vasodilation, and decreased arterial pressure. (2012) showed that mild to moderate increases in hematocrit and blood viscosity did not result in a rise in vascular resistance or blood pressure, but actually caused the opposite effect. One of the most important molecules that promotes an augmentation in vascular diameter (i.e., vasodilation) is nitric oxide (NO). This is because vessels are not rigid tubes they can change their diameters in response to various physiological stimuli. However, several works conducted in the past 10–15 years have shown that, in a physiological context, the parameters of this equation cannot be considered to be truly independent of each other. The dimensions of the vascular system (most notably the radius, which is raised to the fourth power) play a more important role in determining vascular resistance than blood viscosity does. When applying Poiseuille’s Law to the cardiovascular system, one must consider the radius and the length of the vessels, and the viscosity of the blood. Moreover, regular physical exercise has been shown to decrease blood viscosity in sickle cell mice, which could be beneficial for adequate blood flow and tissue perfusion. While acute, intense exercise may increase blood viscosity in healthy individuals, recent works conducted in sickle cell patients have shown that light cycling exercise did not cause dramatic changes in blood rheology. This paradox seems to be due to the fact that in SCD RBC with the highest deformability are also the most adherent, which would trigger vaso-occlusion. However, while the deformability of RBC decreases during acute vaso-occlusive events in SCD, patients with the highest RBC deformability at steady-state have a higher risk of developing frequent painful vaso-occlusive crises. 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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