Prostanoids lhat:

• maintain Gl mucosal integrity -promote edema

• inhibit neutrophil adherence • promote fever

• maintain renal blood flow • promote pain

• promote platelet aggregation (TXAa)

Figure 2 Arachidonic acid is metabolized by the enzyme cyclo-oxygenase (COX) to form prostaglandins. It has been suggested that the COX-1 isoform is responsible for producing prostaglandins important to the function of the gastrointestinal (Gl) tract, kidney and platelet, while COX-2 is expressed at sites of inflammation and produces the prostaglandins that contribute to the associated pain, swelling and redness. Currently marketed NSAIDs show little selectivity for COX-1 versus COX-2, perhaps explaining their detrimental effects on the gut and kidney when used at doses required to reduce inflammation.

been shown to be the predominant form of COX expressed at sites of inflammation. This has given rise to the hypothesis that NSAIDs reduce inflammation through their inhibitory effects on COX-2, while producing their toxicity in the gastrointestinal tract and kidney through inhibitory effects on COX-1. If this is true, highly selective inhibitors of COX-2 should produce the beneficial effects of NSAIDs without the toxicity they exhibit in some tissues. This hypothesis is supported by considerable data, although there is evidence of prostaglandins derived from COX-2 performing important physiological functions in some circumstances, such as in situations in which the gastrointestinal tract is inflamed (see below).

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