The effect of indomethacin and dexamethasone on an allergic inflammation in rats, a novel model of allergic inflammation of an air pouch type, was examined. Indomethacin and dexamethasone exerted a dose-dependent inhibition of both the accumulation of inflammatory exudate and the migration of leukocytes into the exudate. And although prostaglandin E₂ levels in the exudate were lowered to the same extent by treatment with indomethacin and dexamethasone, inhibition of both exudate accumulation and leukocyte migration was more pronounced after treatment with dexamethasone. The differences in the effectiveness of indomethacin and dexamethasone in terms of inhibition of arachidonate metabolism in the allergic air pouch inflammation are discussed.

Abstract-The effect of piroxicam on polymorphonuclear neutrophils (PMN) functions induced by several stimuli was evaluated in vitro. Preincubation of rabbit or human PMN with piroxicam inhibited the cellular responses elicited by N-formylmethionyl-leucyl-phenylalanine (FMLP) such as superoxide anion (O2-) generation, granule enzyme release and chemotaxis. The effectiveness of piroxicam on each response was superior to those of indomethacin and ibuprofen. Also when either concanavalin A, zymosan-treated serum or ionophore A23187 was used as stimuli, piroxicam inhibited O2-generation of PMN. The inhibitory effect of piroxicam on FM LP-induced O2-generation was dependent on the concentration of stimuli and was reversed, by increasing the extracellular calcium concentration.In addition, piroxicam had no effect on the activity of a chymotrypsin-like esterase, N-acetylphenylalanine-8-naphthyl esterase, isolated from rabbit PMN. These results suggest that at least some of the anti-inflammatory effects of piroxicam may be mediated by affecting PMN functions, and the inhibition of Of generation of PMN by piroxicam may be related to its capacity to modulate the association of calcium with these cells.

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