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Abstract

Blood rheology properties-including whole blood viscosity, plasma viscosity, and red blood cell (RBC) deformability and aggregation—are key regulators of blood flow and vascular function. Blood viscosity increases blood flow resistance but also contributes to shear stress, a key determinant of vascular resistance and diameter. RBC deformability and aggregation underlie the shear-thinning behavior of blood, allowing blood viscosity to adjust with changing shear rates. However, the extent to which blood rheology regulates blood flow in humans remains poorly understood. This dissertation aimed to examine how acute elevations in blood viscosity (Study 1) and RBC deformability (Studies 2 and 3) influence vascular perfusion and reactivity under distinct physiological and environmental conditions, including plasmapheresis, plasma contraction, exercise, and chronic hypoxia. In separate trials, study 1 induced hemoconcentration through plasma donation (via plasmapheresis) and diuresis (via oral furosemide) to assess its effects on brachial artery blood flow and reactive hyperemia flow-mediated dilation (RH-FMD). While increased blood viscosity did not alter brachial artery blood flow or RH-FMD, plasma donation and not diuresis enhanced microvascular function, as assessed by reactive hyperemia. Study 2 examined the impact of handgrip exercise and phosphodiesterase-5 inhibition (PDE5) with sildenafil citrate on RBC deformability, brachial artery blood flow, and cerebral blood flow (CBF). Exercise increased RBC deformability, and PDE5-i prolonged this elevated deformation; however, these changes did not affect basal CBF, brachial artery blood flow, or handgrip-induced exercise hyperemia. Study 3 evaluated the effects of pentoxifylline, a non-specific PDE inhibitor, on blood rheology, cardiac output, and CBF at high altitude. Chronic hypoxia increased blood viscosity and reduced RBC deformability, but pentoxifylline had no significant effect on blood rheology, CBF or cardiac output. In summary, while physiological and environmental stressors altered blood rheology, these changes did not significantly influence blood flow or vascular reactivity in healthy individuals.