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Kinetics of platelet adhesion to a fibrinogen-coated surface in whole blood under flow conditions
ZA. Gabbasov, YN. Avtaeva, IS. Melnikov, SD. Okhota, M. Caprnda, I. Mozos, R. Prosecky, L. Rodrigo, P. Kruzliak, NI. Zozulya
Language English Country United States
Document type Journal Article
Grant support
21-15-00029
Russian Science Foundation
NLK
Directory of Open Access Journals
from 2019
PubMed Central
from 1997
Europe PubMed Central
from 1997
ProQuest Central
from 2019-03-01
Medline Complete (EBSCOhost)
from 2012-01-01
Health & Medicine (ProQuest)
from 2019-03-01
Public Health Database (ProQuest)
from 2019-03-01
Wiley Free Content
from 1996
Wiley-Blackwell Open Access Titles
from 2019
PubMed
34347925
DOI
10.1002/jcla.23939
Knihovny.cz E-resources
- MeSH
- Platelet Adhesiveness * MeSH
- Platelet Aggregation MeSH
- Fibrinogen metabolism MeSH
- Platelet Aggregation Inhibitors pharmacology MeSH
- Kinetics MeSH
- Humans MeSH
- Platelet Glycoprotein GPIb-IX Complex antagonists & inhibitors metabolism MeSH
- Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors metabolism MeSH
- Blood Platelets metabolism MeSH
- Healthy Volunteers MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
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.
Department of Functional Sciences Victor Babes University of Medicine and Pharmacy Timisoara Romania
Faculty of Medicine University of Oviedo and Central University Hospital of Asturias Oviedo Spain
Institute of Biomedical Problems of Russian Academy of Sciences Moscow Russia
References provided by Crossref.org
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- $a 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.
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