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  • Title: New trends in clinical hemorheology: an introduction to the concept of the hemorheological profile.
    Author: Stoltz JF, Donner M.
    Journal: Schweiz Med Wochenschr Suppl; 1991; 43():41-9. PubMed ID: 1843037.
    Abstract:
    It has now been clearly established that blood behaves like a non-Newtonian fluid exhibiting specific features with the probable existence of a plasticity threshold, a viscosity that varies as a function of shear rate and a non-homogeneous nature of the medium during flow. When apparent blood viscosity is represented as a function of shear rate, a high viscosity is observed at low shear rates, mainly due to rouleaux formation or red cell aggregates. At high shear rates, viscosity decreases. Apparent blood viscosity is mainly dependent on the following parameters: cell volume concentration (hematocrit); plasma viscosity (which is itself dependent on the type and concentration of the proteins); mechanical properties of the red cells, the main determinants being the cell membrane and internal viscosity; red blood cell aggregation; shear stress applied. Pathological changes in one of the factors controlling blood viscosity and the resulting clinical symptoms constitute the hyperviscosity syndromes. The field of hyperviscosity syndromes concern the situations where the increased blood viscosity and the accompanying modifications in flow resistance must be considered as being the result of the overall rheological behaviour of blood. In this general context, hyperviscosity syndromes can be divided into 4 main groups: 1. Increase in the number of blood cells (mainly red cells) 2. Increase in the plasma protein concentrations or the appearance of high amounts of a monoclonal protein 3. Increase in internal red cell viscosity or a change in the mechanical properties of the erythrocyte membrane 4. Increase in erythrocyte aggregation (formation of barely or in no way dissociable aggregates). Considered from a hemodynamic viewpoint, the appearance of a hyperviscosity syndrome could (by 'feed back' mechanisms) enhance the phenomenon and slow down blood flow or even stop flow completely, thus making ischemia and thrombosis easier. Further, the appearance of the syndrome also results in a decrease in the blood's overall oxygen transport capacity, which, at a primary approach, is proportional to the ratio hematocrit/blood viscosity.
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