Abstract
The apparent viscosity (η) of blood is determined by plasma viscosity, hematocrit (Hct), cell deformation and cell aggregation. The optimum Hct for oxygen transport varies with shear conditions and shows regional differences. In circulation in vivo, the complex geometry causes inertial, in addition to viscous, losses. Microvessels have low Hct and correspondingly low η. Hydrodynamic interactions between red blood cells (RBCs) and white blood cells (WBCs) may contribute to WBC adhesion to the endothelium. Entry of WBC into diverging branches may cause redistribution of RBCs. There is some understanding of the relation between in vitro and in vivo blood rheology, but further investigations are needed.
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