Synthesis of thromboxane a2 is inhibited by Aspirin , which is often recommended in low doses for people at risk for coronary heart disease and/or stroke.
Aspirin inhibits both the potent platelet thromboxane A2 and the potent anti-aggregator prostacyclin. Another method to prevent platelet aggregation may be to selectively reduce thromboxane synthesis.
Aspirin reduces the production of thromboxane A2, which is responsible for platelet aggregation, via inhibiting cyclooxygenase. Ticlopidine blocks the platelet membrane's ability to perform its function by preventing ADP-induced platelet-fibrinogen binding and subsequent platelet-platelet interaction. While thromboxane A2 promotes platelet aggregation, prostacyclin inhibits it.
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