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.