Related Experiment Video
Updated: Aug 12, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Inhibition of surface-induced platelet activation by nitric oxide
M K Sly1, M D Prager, R C Eberhart
1Department of Surgery, University of Texas Southwestern Medical Center at Dallas 75235, USA.
Abstract:
This study was undertaken to determine whether the nitric oxide/platelet cyclic guanosine monophosphate (NO/cGMP) pathway might be used to reduce platelet activation by artificial surfaces. Because serotonin release (SR) is a platelet activation indicator, rabbit platelets in their own plasma (PRP) were labeled with 3H-serotonin. Labeled PRP was incubated with glass beads for 5-10 min, at 37 degrees C with gentle agitation, and SR was measured. PRP pretreatment with NO gas or nitroprusside + N-acetylcysteine inhibited SR 50%. Dose response studies indicate the existence of an optimal NO concentration above which its inhibitory effect is diminished. The guanylate cyclase inhibitor methylene blue attenuates the NO effect, implicating cGMP in NO mediated inhibition of surface induced platelet activation. Adult pigs were supported on a membrane oxygenator in an in vitro model of cardiopulmonary bypass (CPB). Introduction of NO gas into the oxygenator sweep gas at 500 ppm reduced platelet adherence to the oxygenator surfaces, increased circulating platelet counts, and decreased the rate of platelet aggregation (whole blood impedance platelet aggregometry) compared with the results of the control animals. Indications of NO toxicity were seen when the NO flow rate was increased to 1,000 ppm. These studies support the hypothesis that NO reduces platelet activation by artificial surfaces in clinical devices.
Related Concept Videos
Nitric Oxide Signaling Pathway
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Clot Retraction and Fibrinolysis
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

