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Kinetics of platelet adhesion to a fibrinogen‐coated surface in whole blood under flow conditions

AIM: To test a novel method of assessment of platelet adhesion to a fibrinogen‐coated surface in whole blood under flow conditions. METHODS: We developed a fluidic device that mimics blood flow in vessels. The method of detection of platelet adhesion is based on recording of a scattered laser light...

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Detalles Bibliográficos
Autores principales: Gabbasov, Zufar A., Avtaeva, Yuliya N., Melnikov, Ivan S., Okhota, Sergey D., Caprnda, Martin, Mozos, Ioana, Prosecky, Robert, Rodrigo, Luis, Kruzliak, Peter, Zozulya, Nadezhda I.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8418503/
https://www.ncbi.nlm.nih.gov/pubmed/34347925
http://dx.doi.org/10.1002/jcla.23939
Descripción
Sumario:AIM: To test a novel method of assessment of platelet adhesion to a fibrinogen‐coated surface in whole blood under flow conditions. METHODS: We developed a fluidic device that mimics blood flow in vessels. The method of detection of platelet adhesion is based on recording of a scattered laser light signal from a fibrinogen‐covered surface. Testing was performed in platelet‐rich plasma (PRP) and whole blood of healthy volunteers. Control measurements were performed, followed by tests with inhibition of platelet GPIIa/IIIb and GPIb receptors. Then, the same testing sequence was performed in whole blood of persons with autoimmune thrombocytopenia and type 3 von Willebrand disease. RESULTS: The change in intensity of scattered light was 2.7 (2.4; 4.1) times higher in whole blood (0.2 ± 0.08V, n = 7) than in PRP (0.05 ± 0.02 V, n = 7), p < 0.01. The blocking of GP IIb/IIIa receptors decreased the intensity of scattered light to 8.5 (6.5;12)%; the blocking of GPIb receptors decreased it to 34 (23;58)%, p < 0.01. In the whole blood of a person with autoimmune thrombocytopenia, the inhibition of GPIb receptors decreased platelet adhesion, but no effect was observed in type 3 von Willebrand disease. Inhibition of platelet GPIIb/IIIa receptors alone or combined inhibition of GPIb and GPIIb/IIIa receptors resulted in almost total suppression of adhesion in both cases. CONCLUSION: Our system effectively registers platelet adhesion to a fibrinogen‐coated surface under controlled‐flow conditions and may successfully be applied to the investigation of platelet adhesion kinetics.