Mode of Action

Acetylsalicylic acid (ASA ) irreversibly inhibits the cyclooxygenase and thus prevents the conversion of arachidonic acid to thromboxane A2 (TxA2). This effect translates into the inhibition of thromboxane A2-dependent platelet aggregation and vasoconstriction.

Ticlopidine and clopidogrel interfere with the signal transduction triggered by binding of ADP to its platelet receptor.
ADP released from activated platelets is rapidly metabolised to adenosine monophosphate (AMP) and adenosine. Adenosine is a potent inhibitor of platelet aggregation similar to prostacyclin (PgI2).

Dipyridamole effectively inhibits the uptake of adenosine into cells (red blood cells, platelets, endothelial cells). Thus dipyridamole increases the local concentration of adenosine, which accumulates in the microenvironment of a growing thrombus.

GP IIb/IIIa antagonists block the binding of fibrinogen and other ligands to the platelet GP IIb/IIIa receptor. They inhibit platelet aggregation independently of the nature of the proaggregatory stimuli.

Multiple Mechanisms of Enhanced Tissue Perfusion