ASPIRIN DOES NOT AFFECT THE NOW CYTOMETRIC DETECTION OF FIBRINOGEN BINDING TO, OR RELEASE OF ALPHA-GRANULES OR LYSOSOMES FROM, HUMAN PLATELETS

1. Aspirin inhibits the conversion of arachidonic acid to thromboxane A(2) which reinforces the effects of weak agonists such as ADP in plat elets. 2. In this study the effect of aspirin (300 mg/day) on platelet agonist response was measured by whole blood flow cytometry of unfixe d blood samples from normal subjects (n = 10), an assay that investiga tes aggregation-independent changes in the platelet. 3. Fibrinogen bin ding to unstimulated platelets or to platelets stimulated with ADP or thrombin was unaffected by aspirin. 4. Under the conditions of this as say, platelets undergo a partial degranulation of alpha-granules and l ysosomes (evidenced by expression of P-selectin and CD63, respectively ) in response to ADP, and full degranulation in response to thrombin. P-selectin expression was paralleled by release of beta-thromboglobuli n. None of these events was affected by aspirin. 5. Thromboxane format ion was totally prevented by the aspirin treatment, as shown by Born a ggregometry in which the platelet aggregatory response to arachidonic acid was abolished and secondary aggregation by ADP was inhibited. 6. The flow cytometric assay can therefore be used to investigate platele ts in patients, regardless of aspirin therapy. 7. These findings sugge st that platelet fibrinogen binding and the release of platelet alpha- granule and lysosomal contents, in response to stimulation with physio logical agonists, can continue in patients despite aspirin therapy. Th is may help to explain why aspirin is only partially effective in prev enting thrombotic events.