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Aspirin does not inhibit adenosine diphosphate-induced platelet alpha-
granule release
CS Rinder, LA Student, JL Bonan, HM Rinder and BR Smith
Department of Anesthesiology, Yale University School of Medicine, New
Haven, CT 06510.
The involvement of metabolites of arachidonic acid in platelet-dense
granule secretion and secondary platelet-platelet interactions is well
characterized. However, their role in heterotypic interactions dependent on
alpha-granule secretion is less well understood. Using platelet-surface
expression of P-selectin as a marker of alpha-granule secretion, we have
shown that: (1) aspirin treatment of platelets at doses that block dense
granule secretion does not inhibit alpha-granule secretion to adenosine
diphosphate (ADP); (2) synergism between epinephrine and ADP in the
induction of P-selectin expression is similarly unaffected by aspirin; and
(3) the ability of P-selectin to mediate adhesion of activated platelets to
monocytes and polymorphonuclear lymphocytes in whole blood is also
unchanged by aspirin treatment. To further explore the mechanisms
responsible for platelet alpha-granule secretion, we have shown that
inhibition of Na+/H+ exchange by either acidification of the extracellular
medium or amiloride treatment blocked ADP-induced P-selectin expression. In
contrast, incubation with the platelet lipoxygenase inhibitor 5,8,11-
eicosatrynoic acid, by itself and with aspirin, did not decrease ADP-
induced P-selectin expression. We conclude that platelet alpha-granule
secretion in response to ADP is dependent on intact Na+/H+ exchange but is
independent of the lipoxygenase- and cyclooxygenase-dependent metabolites
of arachidonic acid.
Volume 82,
Issue 2,
pp. 505-512,
07/15/1993
Copyright © 1993 by The American Society of Hematology

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