Nonsteroidal Antiinflammatory Drugs: A Review

Abstract

The increasing use of nonsteroidal antiinflammatory drugs (NSAIDs) in small animals has resulted in the development of new and innovative additions to this class of drugs. Examples of NSAIDs now available for use in small animals include aspirin, etodolac, carprofen, ketoprofen, meloxicam, deracoxib, and tepoxalin. The purposes of this article are to review the pathophysiology of prostaglandin synthesis and inhibition, the mechanisms of action, pharmacokinetics, pharmacological effects, and potential adverse reactions of aspirin and the newly released NSAIDs.

Effects of Tepoxalin and Medetomidine on Glomerular Filtration Rate in Dogs

“…Prostaglandins (PGs) may be synthesized in response to a variety of insults, and these compounds act as mediators contributing to pain and inflammation. Inhibition of the production of PGs synthesized in response to insults can reduce inflammation and provide analgesia [2,6]. PGs having beneficial effects are produced normally in the absence of inflammatory insults and serve to maintain blood flow and function to the renal, hepatic, and cardiovascular systems [2,6,13,29].…”

“…Inhibition of the production of PGs synthesized in response to insults can reduce inflammation and provide analgesia [2,6]. PGs having beneficial effects are produced normally in the absence of inflammatory insults and serve to maintain blood flow and function to the renal, hepatic, and cardiovascular systems [2,6,13,29]. Documented adverse effects of NSAIDs are a result of the ability of these agents to inhibit the production of beneficial PGs as well as those mediating inflammation.…”

“…The NSAIDs may inhibit one or more of several pathways of PG formation. The cyclooxygenase-1 (COX-1) pathway produces PGs that are constitutive and have activity in renal arterioles, collecting ducts, and glomeruli as well as in many other organs [6]. These COX-1-derived PGs function to maintain blood flow and function to a variety of tissues.…”

“…The COX-2 pathway is inducible, and the effects of its PG end products on the kidney differ depending upon species. The COX-2-derived PGs are thought to be generated primarily due to the effects of inflammation [2,6,13,29]. Highly COX-2 selective NSAIDs are not always associated with minimal effects on renal function [29].…”

Letter to the Editor

“…Deracoxib is a COX-2 selective NSAID that is indicated for osteoarthritis and postoperative orthopedic pain due to inflammation. 5 However, BMAs are thought to cause minimal inflammatory pain; instead, the pain reported by humans is characterized as sharp, intense and piercing. In addition, according to the manufacturer's label, the bioavailability of Deracoxib is significantly reduced unless given with food, which was not done in this study.…”