Does acetylsalicylic acid ingestion inhibit ADP-induced secondary aggregation and other platelet functions in normal subjects?
Acetylsalicylic acid (aspirin) acutely abolishes secondary platelet aggregation and serotonin release induced by ADP, providing mechanistic evidence for its antiplatelet effects.
SummarySecondary aggregation of platelets was produced in 8 of 10 normal subjects by a critical concentration of adenosine diphosphate (ADP) ranging from 1.0-2.0 μM. Shortening of the Russell Viper Venom clotting time and release of serotonin-14C were also observed with the critical concentration of ADP or with higher levels, but did not occur in the two subjects who showed only primary aggregation in response to ADP. Ingestion of 1.3 gm of acetylsalicylic acid in a divided dose 1 and 2 hours prior to testing abolished secondary aggregation, serotonin release, and platelet factor-3 activation induced by ADP, as well as aggregation and serotonin release induced by connective tissue particles, but did not affect primary ADP-induced aggregation.
Zucker et al. (Thu,) studied this question.