An enzymatic mechanism for the antithrombotic and antihemostatic actions of aspirin.
Aspirin-type drugs may inhibit irreversible clumping of human blood platelets by blocking the enzymatic conversion of arachidonic acid to a hitherto undiscovered factor, labile aggregation-stimulating substance, which triggers aggregation and to prostaglandin E(2), which sensitizes the platelets to its aggregatory effects.
D001095:Arachidonic Acids / Q000378:metabolism*; D001241:Aspirin / Q000494:pharmacology*; D001779:Blood Coagulation Factors / Q000096:biosynthesis*; D001792:Blood Platelets / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D006899:Mixed Function Oxygenases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010973:Platelet Adhesiveness / Q000187:drug effects*; D011453:Prostaglandins / Q000096:biosynthesis* / Q000494:pharmacology
D001095:Arachidonic Acids; D001779:Blood Coagulation Factors; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins; D006899:Mixed Function Oxygenases; D001241:Aspirin; D007213:Indomethacin