Mechanisms of action: aspirin.
Aspirin, one of the oldest antiplatelet agents used for antithrombotic therapy, has been demonstrated to cause acetylation of the cyclo-oxygenase and irreversible inhibition of thromboxane synthesis for the life of the platelet. Aspirin has a similar effect upon the endothelial cyclo-oxygenase, but in contrast to that of the platelet, it is less sensitive and has the capacity to generate new cyclo-oxygenase activity if aspirin is removed from the system. Other non-steroidal anti-inflammatory agents such as ibuprofen react in a reversible manner with either the platelet or the endothelium and may actually "protect" the cyclo-oxygenase against aspirin or other agents which interact with the cyclo-oxygenase. Aspirin may act in other ways to exert an antithrombotic effect, but cause and effect relationships have not yet been demonstrated.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors; D004727:Endothelium / Q000378:metabolism; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D012459:Salicylates / Q000494:pharmacology; D020156:Salicylic Acid; D013931:Thromboxanes / Q000378:metabolism
D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D012459:Salicylates; D013931:Thromboxanes; D016718:Arachidonic Acid; D020156:Salicylic Acid; D001241:Aspirin; D007052:Ibuprofen; D007213:Indomethacin