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Abstract
Dazoxiben, a thromboxane synthase inhibitor, inhibits arachidonic acid induced aggregation
in platelet-rich plasma from some donors only ("responders"). We have studied the
effect of dazoxiben in vitro on platelet aggregation and prostaglandin (PG) metabolism
and the influence of the incubation period and of exogenously added serum albumin
(SA). SA, which increases the production of anti-aggregatory PGD2 from cyclic endoperoxides,
induced "non-responder" human platelets to respond. With rabbit platelets, however,
that are insensitive to PGD2, exogenous SA failed to potentiate dazoxiben-induced
inhibition. The ratio between PGD2 and TXB2 + PGE2 formed was crucial in determining
the response of human platelets to dazoxiben: whenever this ratio was high, platelet
aggregation was inhibited. SQ 22536, an adenylate cyclase inhibitor, and NO164, a
PGD2 antagonist, reversed the inhibition by dazoxiben in human platelet-rich plasma,
stressing the importance of a PGD2 mediated rise of cyclic AMP for the effectiveness
of a thromboxane synthase inhibitor.