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Platelet-derived NO slows thrombus growth on a collagen type III surface by Robert H Williams; Matthias U Nollert is a Medicine article available to read on EtoBox.

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Nitric oxide (NO) is a free radical that plays an important role in modulating platelet adhesion and aggregation. Platelets are a source of vascular NO, but since erythrocytes avidly scavenge NO, the functional significance of platelet-derived NO is not clear. Our purpose was to determine if NO from platelets affects platelet thrombus formation in the presence of anticoagulated whole blood in an __in vitro__ parallel plate flow system. We studied platelet adhesion and aggregation on a collagen type III surface in the presence of physiologically relevant fluid mechanical shear stress. We found that certain receptor mediated agonists (insulin and isoproterenol) caused a concentration dependent reduction in thrombus formation at a shear rate of 1000 s^-1^. This effect was mediated by NO since it was abolished in the presence of the NO inhibitor L-nitro-arginine-methyl-ester (L-NAME). As expected, at venous levels of shear rate (100 s^-1^) neither of the agonists had any effect on thrombus formation since platelet adhesion does not depend on activation at these low levels of shear. Interestingly, at a shear rate of 2000 s^-1^ the addition of L-NAME caused an increase in platelet covera

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Author

Robert H Williams; Matthias U Nollert

Publisher

BioMed Central; Springer (Biomed Central Ltd.); [London]: BioMed Central, 2003-; Springer Science and Business Media LLC; Society for Mining, Metallurgy and Exploration Inc. (ISSN 1477-9560)

Published

2004

Language

EN

Field

Medicine (Health Sciences)