Why the study?
Does a nitric oxide-releasing dextran derivative reduce platelet activation and clotting in blood plasma?
Does a nitric oxide-releasing dextran derivative reduce platelet activation and clotting in blood plasma?
A novel NO-releasing dextran derivative significantly reduces platelet adhesion and activation in vitro, suggesting potential as an anti-platelet therapeutic agent for cardiovascular interventions.
May inform development of NO-releasing biomaterials for thrombosis prevention; leaves open translation from this in vitro model.
Controlling platelet activation and clotting initiated by cardiovascular interventions remains a major challenge in clinical practice. In this work, the anti-thrombotic properties of a polysaccharide-based nitric oxide (NO)-releasing dextran derivative are presented. Total platelet adhesion, platelet morphology and whole blood clotting kinetics were used as indicators to evaluate the anti-clotting properties of this material. With a total NO delivery of 0.203±0.003 μmol, the NO-releasing dextran derivative (Dex-SNO) mixed with blood plasma demonstrated a significantly lower amount of platelet adhesion and activation onto a surface and reduced whole blood clotting kinetics. Nearly 75% reduction in platelet adhesion and a significant retention of platelet morphology were observed with blood plasma treated with Dex-SNO, suggesting this to be a potential anti-platelet therapeutic agent for preventing thrombosis that does not have an adverse effect on circulating platelets.
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Damodaran et al. (2013) studied this question.
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