Aspirins Unique Effect on Platelet Physiology

Because aspirin blocks prostanoid synthesis, the ability of aspirin to impair platelet 

A Anudeate target B Exquisite sensitivity C Permanent, limited effect 

Aspirin s permanent inactivation of the anucleate platelet is also responsible for the cumulative effect seen with repeated daily dosing below 100 mg (25). Daily administration of 30 to 50 mg of aspirin has been shown to lead to complete suppression of platelet thromboxane synthesis in 7 to 10 days (25, 30, 31). This, in turn, leads to inhibition of platelet aggregation and prolongation of the bleeding time, a clinical test often useful in identifying patients with platelet functional defects for further study and characterization (28,32). 

Nucleated cells such as endothelium can replace their cyclooxygenase supply following aspirin treatment by synthesizing new enzyme. This ability to recover from aspirin treatment contributes to the reduced aspirin sensitivity of these cells as compared with platelets (25,28). 

How Aspririn-Mediated Cyclooxygenase Inhibition Prevents Arterial Thrombosis 

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