It is has been known for more than 80 years that compared to in vitro determinations, blood behaves as a less viscous fluid under in vivo flow conditions. The experiments of Whittaker and Winton were among the first dealing with the in vivo effects of altered blood rheology, and experimental studies during the second half of 20th century have provided additional evidence for the complexity of in vivo hemodynamics–hemorheology relationships. Careful studies indicate that the impact of a given blood rheology alteration is determined by the properties of the experimental model (e.g., organ or tissue under investigation), experimental approach (e.g., intravital microscopy, whole organ perfusion) and method used to modify blood rheology. In addition, vascular control mechanisms may play a major role in the resulting hemodynamic effects of a hemorheological alteration: (1) a response simply related to metabolic autoregulation in which there is a compensatory vasodilation due to altered in vivo blood flow and organ/tissue hypoxia; (2) modulation of endothelial function (e.g., NO production) via altering wall shear stress, thereby leading to changes of vascular hindrance. The in vivo effects of altered red blood cell (RBC) aggregation have been investigated in various experimental models. A novel technique for modifying RBC aggregability (i.e., intrinsic tendency of RBC to aggregate) by covalent attachment of specific co-polymers has been used in some studies, and has provided data reflecting the specific effects of RBC aggregation without the influence of altered suspending phase properties. These data indicate that both the magnitude of the hemodynamic effect and the direction of the alteration depend on the intensity of RBC aggregation. Using the same novel technique, RBC aggregation has been shown to be an important determinant of endothelial function through its effects on RBC axial distribution and wall shear stress. These somewhat diverse findings can be explained by considering the contribution of various in vivo hemorheological mechanisms that have opposite effects on in vivo flow resistance.
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