Aspirin - Mechanism of Action

Acetylsalicylic acid (Brand names: Aspirin, Aspro, Aspegic, Alka Seltzer, Aspirin Cardio, cardioaspirine, Cardiopirin, Cardipirin, among others) is a nonsteroidal antiinflammatory drug (NSAID) used for treating pain, fever, arthritis and other types of inflammation. Acetylsalicylic acid may also be used to reduce the risk of heart attack.

Two forms of cyclooxygenase have been described in mammals:
  • The constitutive cyclooxygenase, COX-1, synthesizes prostaglandins necessary for normal gastrointestinal and renal function.
  • The inducible cyclooxygenase, COX-2, is responsible for the production of mediators including PGE2 which induce pain, inflammation or fever
Aspirin inhibits both types of cyclooxygenases (COX-1 and COX-2).

Aspirin has two main actions in the body:
  • Anti-prostaglandin: Aspirin inhibits irreversibly the enzyme, cyclooxygenase (COX), an early component of the arachidonic acid cascade, resulting in the reduced formation of prostaglandins and thromboxanes. Prostaglandins act as messenger molecules in the process of inflammation; hence aspirin acts as an anti-inflammatory and pain reliever agent in this process.
  • Anti-platelet (blood thinner agent): COX also plays a role in cessation of bleeding. Blood clotting is the result of a complex mechanism which involves many different cells, including a type known as platelets. COX activates a chemical known as thromboxane A2 that causes platelets to stick together. By inhibiting the cyclooxygenase (COX), Aspirin blocks platelet production of thromboxane A2 and thereby, platelet activation and aggregation. This property accounts for its use in the long-term prevention of heart attacks. The inhibitory effect of Aspirin on platelet thromboxane production persists for the lifespan of the platelet, around 7 to 10 days.
Inhibition of COX-1 is associated with the gastrointestinal and renal toxicity of Aspirin. © 2014 - All videos published on MedVideos are the property of their respective authors or publisher.