TITLE

Blood Fluidity as a Consequence of Red Cell Fluidity: Flow Properties of Blood and Flow Behavior of Blood in Vascular Diseases

AUTHOR(S)
Schmid-Sch�nbein, H.; Rieger, H.; Fischer, T.
PUB. DATE
May 1980
SOURCE
Angiology;May1980, Vol. 31 Issue 5, p301
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Blood is known to be an extremely non-Newtonian material, the fluidity (or reciprocal of viscosity) of which can vary in vivo between that of plasma alone and zero, that is, the total lack of fluidity in the absence of coagulation. The fluidity of blood under high driving pressures and in small blood vessels is unusually high when compared to that of all other known suspensions or emulsions. The high fluidity of blood is caused by the fluidity of the red cells, which adapt to the forces of flow and participate in flow much like fluid droplets. When subjected to high forces the blood behaves dynamically like an emulsion of extremely low viscosity. In the absence of adequate flow forces, the erythrocytes are aggregated into rouleaux and rouleaux networks, which render to blood the properties of a reticulated suspension. Under these flow conditions, the fluidity of blood strongly decreases if the hematocrit value is normal or slightly elevated. If the flow forces fall below a critical level, the fluidity approaches zero, under which conditions the flow of blood ceases altogether (despite the presence of residual driving pressures). The fluidity of blood is further jeopardized by an enhanced tendency to aggregation and biochemical erythrocyte rigidification, for example, by lactacidosis, hyperosmolarity, or loss of ATP. However, an actual loss of fluidity under these conditions occurs only if the biochemical changes are strictly associated with a drop in driving pressures (locally or generally). Restitution of blood fluidity can be achieved most simply by isovolumic hemodilution, by defibrinogating agents, or by drugs that protect against rigidifying effects of acidosis or other biochemical sequelae of stagnation anoxia.
ACCESSION #
16390578

 

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