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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Nitric oxide released from activated platelets inhibits platelet recruitment
J E Freedman1, J Loscalzo, M R Barnard
1Whitaker Cardiovascular Institute and Evans Memorial Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
The Journal of Clinical Investigation
|July 15, 1997
Summary
Platelets produce nitric oxide (NO) that slightly reduces platelet activation but significantly inhibits platelet recruitment to thrombi. This suggests NO plays a key role in regulating thrombus formation.
Area of Science:
- Cardiovascular Biology
- Hematology
- Biochemistry
Background:
- Vessel injury and thrombus formation cause ischemic coronary syndromes.
- Activated platelets recruit more platelets to growing thrombi.
- A constitutive nitric oxide synthase (NOS) is present in human platelets.
Purpose of the Study:
- To quantify platelet nitric oxide (NO) production.
- To investigate the role of platelet-derived NO in platelet recruitment.
Main Methods:
- Adapted a NO-selective microelectrode for a platelet aggregometer for simultaneous NO production and aggregation measurement.
- Utilized a novel two-population platelet assay with flow cytometry.
- Administered the NOS inhibitor L-NAME to assess NO's effects.
Main Results:
- L-NAME reduced NO production but only modestly increased platelet aggregation.
- L-NAME significantly enhanced platelet recruitment, cyclic GMP reduction, and serotonin release.
- Flow cytometry showed L-NAME increased P-selectin positive platelets and biotinylated platelet recruitment.
Conclusions:
- Stimulated platelets produce NO that moderately inhibits activation but strongly inhibits recruitment.
- Platelet-derived NO appears to regulate platelet recruitment in thrombus formation.
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