The Effects of the Combined Argatroban/Nitric Oxide-Releasing Polymer on Platelet Microparticle-Induced Thrombogenicity in Coated Extracorporeal Circuits.
Animals
Antithrombins
/ pharmacology
Arginine
/ analogs & derivatives
Blood Platelets
/ physiology
Cell-Derived Microparticles
/ physiology
Extracorporeal Circulation
/ methods
Nitric Oxide
/ pharmacology
Pipecolic Acids
/ pharmacology
Platelet Activation
/ physiology
Polymers
/ pharmacology
Rabbits
Sulfonamides
/ pharmacology
Thrombosis
/ prevention & control
Journal
ASAIO journal (American Society for Artificial Internal Organs : 1992)
ISSN: 1538-943X
Titre abrégé: ASAIO J
Pays: United States
ID NLM: 9204109
Informations de publication
Date de publication:
01 05 2021
01 05 2021
Historique:
entrez:
26
4
2021
pubmed:
27
4
2021
medline:
6
7
2021
Statut:
ppublish
Résumé
Clotting, anticoagulation, platelet consumption, and poor platelet function are major factors in clinical extracorporeal circulation (ECC). We have shown that nitric oxide-releasing (NOReL) coatings prevent thrombosis in a rabbit model of ECC without systemic anticoagulation. Nitric oxide-releasing prevents platelet adhesion and activation, resulting in preserved platelet count and function. Previous work has shown that activated platelets form platelet-derived microparticles (PMPs). These experiments were designed to determine if PMPs can identify platelet function during ECC. The objective of this study is to investigate the effects of NOReL on platelet activation and PMP formation during ECC. Uncoated ECCs, including with and without systemic heparin, and NOReL-coated ECCs, including DBHD/N2O2 and argatroban (AG)/DBHD/N2O2-coated ECCs without systemic heparin, were tested in a 4-hour rabbit thrombogenicity model. Before and after ECC exposure, platelets were stimulated with collagen, and PMPs were measured using flow cytometry. The uncoated ECCs clotted within the first hour, while the NOReL-coated ECCs circulated for 4 hours. During pre-ECC blood exposure, platelets stimulated with collagen produced PMPs. With post-ECC exposure, platelets from uncoated circuits generated less PMPs than baseline (mean ± SDs: 23246 ± 3611 baseline vs. 1300 ± 523 uncoated post circuit, p = 0.018) when stimulated with collagen. However, platelets from the AG/DBHD/N2O2-coated ECCs generated a greater number of PMPs as baseline values (23246 ± 3611 baseline vs. 37040 ± 3263 AG/DBHD/N2O2 post 4 hours circuit, p = 0.023). Blood exposure during ECC results in platelet activation and clotting in uncoated ECCs. The remaining circulating platelets have lost function, as demonstrated by the low PMP formation in response to collagen. AG/DBHD/N2O2-coated ECCs prevented significant platelet activation and clotting, while DBHD/N2O2 trended towards prevention of platelet activation. In addition, function of the circulating platelets was preserved, as demonstrated by PMP formation in response to collagen. These results indicate that PMPs may be an important measure of platelet activation during ECC. Platelet-derived microparticles may provide a simplified way to measure platelet function during clinical ECC.
Identifiants
pubmed: 33902103
doi: 10.1097/MAT.0000000000001256
pii: 00002480-202105000-00015
pmc: PMC8083987
mid: NIHMS1613706
doi:
Substances chimiques
Antithrombins
0
Pipecolic Acids
0
Polymers
0
Sulfonamides
0
Nitric Oxide
31C4KY9ESH
Arginine
94ZLA3W45F
argatroban
IY90U61Z3S
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
573-582Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL128337
Pays : United States
Informations de copyright
Copyright © ASAIO 2020.
Déclaration de conflit d'intérêts
Disclosure: The authors have no conflicts of interest to report.
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