Saturday, April 2, 2011


Mechanism of action:
Aspirin causes the inhibition of COX-1by irreversible acetylation of serine residue on its active site and by causing a developmental failure of thromboxane A2 synthetase leading to the inhibition of Thromboxane-A2 synthesis.
In the whole process, Thrombin, collagen and ADP results in stimulation of platelets causing activation of platelet membrane phospholipids leading to the liberation of arachidonic acid from membrane phospholipids. COX-1 converts arachidonic acid to prostaglandin H2 which is then metabolized to thromboxane-A2 which is then released into plasma to cause a change in the shape of the platelets, release of their granules and promoting the clustering of platelets necessary for rapid formation of hemostatic plug.

Aspirin also causes chemical mediators to influence positively on anti-aggregating properties of prostacyclin (PGI2) leading to further blockage of platelet aggregation.
The inhibitory effect apparently occurs in portal circulation where it is relatively faster. The effect occurs for 7-10 days.
Therapeutic uses:
It is used prophylactically for short duration of cerebral ischemia so that the incidence of myocardial infarction is reduced.
It is used in combination with other drugs such as heparin or clopidogrel.

For myocardial infarction prophylactically it is used as 325mg/day.

Adverse effects:
It may cause hemorrhage leading to hemorrhagic stroke or GI bleeding.
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