ABSTRACT
Nonsteroidal anti-inflammatory drugs (NSAID) block the first step of prostaglandin synthesis by inhibiting cyclooxygenase enzymes. This inhibition reduces the production of inflammatory mediators known to sensitize peripheral nociceptors. Some newer NSAIDs target the cyclooxygenase enzyme which is presumably responsible for the formation of inducible prostaglandins known to mediate inflammation. They achieve this with minimal effect on the cyclooxygenase enzyme mediating the formation of constitutive prostaglandins important for maintenance of homeostasis. Because pain intensity may wax and wane in an individual patient, NSAID therapy should be customized to reflect changing patient analgesic requirements with the goal of using the minimum effective dose. Cats appear more predisposed to the toxic effects of most NSAIDs, especially with prolonged administration. Some NSAIDs, most notably aspirin, reduce platelet function leading to prolonged clotting times. Lipoxin has been identified as one substance responsible for the adaptation of the gastrointestinal tract to mucosal injury.
