What effect occurs when aspirin is administered at low doses?

When aspirin is administered at low doses, the primary and most notable effect is the inhibition of platelet aggregation. Aspirin's mechanism of action involves the irreversibly inactivating cyclooxygenase (COX), specifically COX-1 in platelets. This inactivation prevents the conversion of arachidonic acid to thromboxane A2, a potent promoter of platelet aggregation and vasoconstriction.

The inactivation of COX-1 is significant because it leads to a decreased formation of thromboxane, thereby inhibiting platelet aggregation and reducing the risk of thrombus formation associated with cardiovascular events. At low doses, aspirin selectively inhibits COX-1 in platelets while having a minimal impact on COX-2, which is primarily involved in mediating inflammation and pain.

Thromboxane production would decrease as a direct consequence of COX-1 inactivation, further supporting the effect of preventing platelet aggregation. Therefore, the focus of low-dose aspirin therapy is on its ability to modulate platelet function rather than its anti-inflammatory actions associated with COX-2.