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Effect of blood viscocity on arterial flow induced dilator response
A M Melkumyants1, S A Balashov
1Department of Circulation Biomechanics and Control, USSR Cardiology Research Centre, Moscow.
Insights
Blood viscosity significantly impacts arterial dilation. Lowering blood viscosity reduces dilation, while increasing it enhances the flow-induced arterial response, confirming endothelial shear stress sensitivity.
Area of Science:
- Physiology
- Cardiovascular Research
- Biomedical Engineering
Background:
- Flow-induced arterial dilation is crucial for regulating blood flow.
- The role of blood viscosity in this response remains incompletely understood.
- Endothelial shear stress is a proposed mediator of this dilation.
Purpose of the Study:
- To investigate the effect of blood viscosity on flow-induced dilator responses in conduit arteries.
- To determine if changes in blood viscosity modulate endothelial sensitivity to shear stress.
Main Methods:
- Experiments were conducted on anesthetized cats.
- Femoral artery diameter changes were measured in response to stepwise blood flow increases.
- Blood viscosity was manipulated through hemodilution and hemoconcentration.
- Transmural pressure was stabilized throughout the experiments.
Main Results:
- Hemodilution (reduced viscosity) attenuated flow-induced dilation.
- Hemoconcentration (increased viscosity) augmented flow-induced dilation.
- The observed changes in dilation paralleled the alterations in blood viscosity.
Conclusions:
- Blood viscosity directly influences the magnitude of flow-induced arterial dilation.
- These findings support the hypothesis that endothelial cells' sensitivity to shear stress mediates this response.
- Modulating blood viscosity may represent a therapeutic target for vascular function.
Abstract:
Experiments were designed to determine whether blood viscosity affects flow induced dilator response in conduit arteries. Changes in diameter of the femoral artery of anaesthetised cats evoked by stepwise blood flow increases were recorded at normal blood viscocity, at haemodilution, and at haemoconcentration, under conditions of stabilised transmural pressure. Dilator responses caused by the same increments in flow rate increased at haemoconcentration and decreased at haemodilution, in parallel with the changes in blood viscocity. These data show that haemodilution attenuates and haemoconcentration augments flow induced dilatation, and they confirm the suggestion that flow induced arterial dilatation is due to endothelial sensitivity to shear stress.