Open AccessKinetics of platelet adhesion to a fibrinogen‐coated surface in whole blood under flow conditions
Author(s) -
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.
Publication year - 2021
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23939
Subject(s) - fibrinogen , platelet adhesion , platelet , kinetics , adhesion , blood flow , flow (mathematics) , chemistry , biophysics , immunology , medicine , mechanics , biochemistry , biology , physics , classical mechanics , organic chemistry
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.