Hemorheology and vascular control mechanisms

Clin Hemorheol Microcirc. 2004;30(3-4):169-78.

Abstract

Blood rheology is a well-known determinant of tissue perfusion and, according to the Poiseuille relation, hemodynamic resistance in a constant-geometry vascular network is directly proportional to blood viscosity. However, this direct relationship cannot be observed in all in vivo studies. Further, there are several reports indicating marked differences between the in vivo and ex vivo flow properties of blood. These differences can be explained, in large part, by considering special hemorheological mechanisms (e.g., Fahraeus-Lindqvist effect, axial migration) that are of importance in the microcirculation. Additionally, the influence of altered rheological properties of blood and its components on vascular control mechanisms requires consideration: (1) There is an indirect relation between blood rheology and microvascular tone that is mediated by tissue oxygenation, with a compensatory vasodilation occurring if tissue perfusion is impaired due to hemorheological deterioration; (2) Blood rheology may influence vascular tone through alterations of wall shear stress, which in turn determines endothelial generation of vasoactive substances (e.g., nitric oxide). This latter point is of particular relevance to the field of clinical hemorheology, since enhanced red blood cell aggregation has been shown to affect nitric oxide synthesis and thus control of vascular smooth muscle tone. Such multiple pathways by which hemorheological changes can affect vascular resistance help to explain the continuing difficulty of predicting correlations between in vivo and ex vivo hemorheological behavior; they also suggest the need for continued experimental studies in this area.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Blood Vessels / physiology*
  • Hemorheology / methods*
  • Homeostasis
  • Humans
  • Models, Animal
  • Stress, Mechanical
  • Vascular Resistance / physiology*