How does aspirin function as an antiplatelet agent?

Aspirin functions as an antiplatelet agent primarily by irreversibly inhibiting the enzyme cyclooxygenase (COX). COX is responsible for the conversion of arachidonic acid into thromboxane A2, a potent platelet aggregator and vasoconstrictor. By inhibiting COX, aspirin effectively reduces the synthesis of thromboxane A2, leading to diminished platelet activation and aggregation. This action is critical for preventing thrombus formation in cardiovascular conditions.

The irreversible nature of aspirin's inhibition means that the effects last for the lifespan of the platelet, which is typically about 7 to 10 days. This characteristic of aspirin makes it an effective long-term antiplatelet therapy.

In contrast, the other options do not accurately represent aspirin's mechanism of action. Enhancing thromboxane A2 production would increase platelet aggregation, which is the opposite of what aspirin does. Activating plasminogen is related to fibrinolysis rather than platelet aggregation, and while binding to glycoprotein IIb/IIIa receptors does play a role in preventing platelet aggregation, this is more characteristic of other antiplatelet medications, such as glycoprotein IIb/IIIa inhibitors. Thus, the mechanism of