Effect of dipyridamole alone and in combination with aspirin on whole blood platelet aggregation, PGI2 generation, and red cell deformability ex vivo in man

Abdollah R Saniabadi, Timothy C Fisher, Margaret McLaren, Jill F Belch, Charles D Forbes

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    Abstract

    Study objective - The aim was to investigate the effects of dipyridamole, aspirin, and a combination of dipyridamole plus aspirin on platelet aggregation in whole blood, PG12 generation, and red cell deformability ex vivo.
    Subjects - were 16 male volunteers, aged 22-39 years, mean age, 26.6 years.
    Design - This was a randomised, double blind, placebo controlled trial. The volunteer received each of the following treatments 10 days apart: dipyridamole 200 mg; aspirin 300 mg; dipyridamole 200 mg plus aspirin 300 mg; matched placebos.
    Measurements and main results -Blood was taken for platelet function tests, PGI2 metabolite assay, and red cell deformability before and 2 h after the trial dose was taken. Platelet aggregation was quantified by measuring the fall in single platelet count after stimulation with 2 µg.ml-1 collagen or 50 nM platelet activating factor (PAF), or by rollermixing aliquots of blood to initiate spontaneous aggregation.  The platelet function tests were completed at 37°C within 10 min of venepuncture. The stable metabolite of PG12, 6-keto PGF1a, was measured in
    serum. There was inhibition of spontaneous platelet aggregation by dipyridamole (p<0.004), aspirin (p<O.005), and the combination of dipyridamole plus aspirin (p<O.OOO1) as compared with placebo.  PAF induced platelet aggregation was inhibited by dipyridamole (p<0.002) and the combination of dipyridamole plus aspirin (p<O.OOO1) but aspirin alone had no inhibitory effect. Collagen induced
    platelet aggregation was inhibited by all three treatments: dipyridamole (p<O.O6), aspirin (p<O.OOO1), and the combination of dipyridamole plus aspirin
    (p<O.OOO1). PG12 generation was markedly inhibited by aspirin (p<O.OOO1) and the combination doses (p<O.OOO1) but was unaffected by dipyridamole alone. Of the three active treatments, only dipyridamole alone significantly (p<O.OO1) increased red cell deformability; there was a modest decrease in red cell deformability with aspirin.
    Conclusions - The results with PAF support the view that dipyridamole inhibits platelet activation by more than one mechanism; the effect on collagen
    induced and spontaneous platelet aggregation suggests that the effect of the combination doses is additive and that on red cell deformability the synergy is negative.

    Original languageEnglish
    Pages (from-to)177-183
    Number of pages7
    JournalCardiovascular Research
    Volume25
    Issue number3
    DOIs
    Publication statusPublished - Mar 1991

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