Low-dose aspirin (ASA) renders human platelets more vulnerable to inhibition of aggregation by prostacyclin (PGI2).
Pre-treatment of human, platelet-rich plasma with concentrations of aspirin that produced 50% or less inhibition of aggregation induced by collagen, arachidonic acid or adenosine diphosphate, significantly increased the % inhibition of platelet aggregation by a low concentration of authentic prostacyclin or by prostacyclin-like activity generated by incubation of rat aorta rings in human platelet-poor plasma. Similarly a single aspirin tablet (325 mg) taken orally by human volunteers significantly increased the sensitivity of their platelets to inhibition of aggregation by authentic prostacyclin (8.1 X 10(-10) M) for 2-48 h after ingestion. Statistical significance was lost at 72 h but the trend was still evident. These results support the contention that low doses of aspirin may be efficacious in the therapy of arterial thromboembolism since this could preserve some arterial prostacyclin-generating activity which might be sufficient to inhibit adhesion and aggregation of the aspirin-treated platelets.
D000328:Adult; D000818:Animals; D001011:Aorta / Q000378:metabolism; D001241:Aspirin / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D004357:Drug Synergism; D011464:Epoprostenol / Q000096:biosynthesis / Q000494:pharmacology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013923:Thromboembolism / Q000188:drug therapy
D011453:Prostaglandins; D011464:Epoprostenol; D001241:Aspirin