Abstract
Because blood is a non-Newtonian fluid, its energy dissipation during flow is more complex than that of Newtonian fluids. We have shown that, when flow is reinitiated after a pause comparable to physiologic diastole, that a substantial extra transient shear stress develops. This briefly increased resistance is related in shape and duration to blood thixotropy. Both are linked through their dependence on total shear strain (shear rate × time) and its associated rapidly increasing orthogonal reflectivity to the development of cell orientation as flow is initiated and restored. Studies of blood from diabetic patients suggest that a greater predisposition to aggregation of red blood cells mediated by fibrinogen and other plasma proteins influences the magnitude of this transient resistance. The timing and magnitude of blood’s transient resistance are such that, combined with blood’s shear-thinning, it burdens cardiac systole in the large arteries by an increase as great as ten percent and with a brief local peak excess of more than a third.
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