Abstract
The effects of stress on blood fluidity may be mediated through the sympathetic adrenergic nervous system. We investigated this proposition using a micro-channel array flow analyzer that mimics capillaries to study the effects of adrenergic receptor agonists and antagonists on blood fluidity in male Wistar rats. An α-adrenergic receptor agonist and a β-adrenergic receptor antagonist reduced blood fluidity whereas an α-adrenergic receptor antagonist and β-adrenergic receptor agonist increased blood fluidity. Both the stimulatory and inhibitory effects were larger when EDTA was used as an anticoagulant rather than heparin. The α-adrenergic receptor agonist enhanced platelet aggregation whereas and β-adrenergic receptor agonist reduced aggregation when citrate was used as an anticoagulant in platelet-rich plasma. Blood fluidity is affected by many factors including: hematocrit, platelet aggregation, leukocyte adhesion, and erythrocyte deformability. EDTA blocks platelet aggregation by chelating calcium ions whereas heparin does not. The hematocrit was not affected by any of the adrenergic reagents we examined. We propose that adrenergic receptor-modulating drugs alter blood fluidity through changes in both platelet aggregation and erythrocyte deformability.
