Mechanism of action of Aspirin in MI is?
Ans. is 'a' i.e., Thromboxane A2 synthesis inhibition o Aspirin acetylates and inhibits the enzyme cycloxygenase (Cox) - inactivating it irreversible. o Because platelets are exposed to aspirin in the poal circulation before it is deacetylated during first pass in the liver and because platelets cannot synthesize fresh enzyme (have no nuclei) TXA2 formation is suppressed at very low doses and till fresh platelets are formed. o Aspirin also inhibits COX and PGI2 synthesis in vessel wall. However, since intima cells can synthesize fresh enzyme, activity returns rapidly. o So at low doses TXA2 formation by platelets is selectively suppressed, whereas higher doses may decrease both TXA2 and PGI2 production. Note:- According to KDT, aspirin inhibits TX-synthatase also, but no other book (Goodman & Gilman, Katzung, Laurence, Satoskar) has mentioned this.
Thromboxane A2 synthesis inhibition
Thromboxane A2 synthesis stimulation
Antagonist of adenosine
Stimulation of PGF2 synthesis