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Erythrocytes metabolically enhance collagen-induced platelet responsiveness
via increased thromboxane production, adenosine diphosphate release, and
recruitment
J Valles, MT Santos, J Aznar, AJ Marcus, V Martinez-Sales, M Portoles, MJ Broekman and LB Safier
Hospital La Fe, Valencia, Spain.
Erythrocytes promoted platelet reactivity in a plasma medium, as
demonstrated in an in vitro system that independently evaluated the
biochemistry of platelet activation and recruitment. The prothrombotic
erythrocyte effects were metabolically regulated, as evidenced by lack of
activity of ATP-depleted or glutaraldehyde-fixed erythrocytes. They
occurred in the absence of cell lysis as verified by lactate dehydrogenase
assays, and had an absolute requirement for platelet activation. The
presence of erythrocytes induced a twofold increase in platelet thromboxane
B2 (TXB2) synthesis upon collagen stimulation, indicating that erythrocytes
modulated platelet eicosanoid formation. Cell-free releasates from
stimulated platelet-erythrocyte suspensions, which exhibited increased
recruiting capacity, contained 6.9-fold more ADP and 4.9-fold more ATP than
releasates from stimulated platelets alone. Following aspirin ingestion,
TXB2 formation was blocked, but erythrocyte promotion of platelet
reactivity persisted at those doses of collagen that reinduced platelet
activation. Moreover, when platelet mixtures consisted of as little as 10%
obtained before aspirin plus 90% obtained post-aspirin ingestion,
significant erythrocyte enhancement of platelet reactivity occurred, even
at low agonist concentrations. These erythrocyte effects would decrease the
therapeutic potential of inhibition of platelet cyclooxygenase by aspirin.
The erythrocyte- induced modulation of platelet biochemistry and function
emphasizes the importance of cell-cell interactions in stimulus-response
coupling.
Volume 78,
Issue 1,
pp. 154-162,
07/01/1991
Copyright © 1991 by The American Society of Hematology
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