The vascular endothelium and circulating blood cells are exposed to a hemodynamic environment related to the pulsatile nature of the pressure and blood flow which influence the morphology, the physical properties and the metabolism of the cells. Among these mechanical forces, shear stresses, related to the speed gradients and to the blood viscosity, control vascular vasomotor tone and thrombogenecity, stimulating the production of the endothelial factors of relaxation or contraction, of the coagulation factors or activating erythrocyte and platelet aggregation or disaggregation phenomena. Low shear stress is considered to be a critical factor in the causation of thickening of the arterial wall and in the formation of atheromatous plaques. These plaques develop predominantly in specific parts of the arterial tree where asymmetries in the velocity profiles occur. A close relationship has been found in a large general population between plasma viscosity and thickening of the carotid bifurcation. The blood cells share the same environment as the endothelial cells. Thus, the shear stresses to which the erythrocytes are submitted is a major determinant of the blood viscosity. Shear is also an important physiological parameter regulating platelet aggregation in flowing suspensions. However, in vivo, the response of platelets depends on the balance between activation of the platelets by shear and the same rheological forces acting on the endothelial cells which produce mediators which inhibit this activation in order to maintain blood fluidity.