The effects of 3 conventional antiplatelet regimes, dipyridamole 3 .times. 75 mg/day (D), sulfinpyrazone 4 .times. 200 mg/day (S), acetylsalicylic acid [ASA] 3 .times. 330 mg/day combined with D 3 .times. 75 mg/day (ASA + D), and very low dose ASA 100 mg/day on platelet function were studied in a man following 4 days of treatment. D and S slightly increased mean minimal ADP concentration for irreversible aggregation (n.s. [p = not significant]), S reduced aggregation and thromboxane (TX)B2 formation on low dose collagen (2P .ltoreq. 0.05), ASA and ASA + D increased platelet count (2P .ltoreq. 0.05), increased bleeding time (n.s. for ASA, 2P .ltoreq. 0.05 for ASA + D), abolished irreversible aggregation on ADP, suppressed TXB2 formation on all (2P .ltoreq. 0.001) and aggregation on lower concentrations of collagen (2P .ltoreq. 0.01) and abolished aggregation ant TXB2 formation on arachidonic acid (2P .ltoreq. 0.001). Very low dose ASA suppresses platelet aggregation and TXB2 formation on several stimuli of possible physiologic significance. In the light of a recently proposed critical balance of vascular antiaggregatory prostacyclin and platelet proaggregatory TXA2, very low dose ASA might offer advantages over conventional dosage of ASA and should be evaluated in thromboembolic disorders.