Phospholipase A2 activity in the rat air pouch cavity was determined after induction of a reverse passive Arthus reaction. Time-course of phospholipase A2 activity appeared to correlate with increased prostaglandin E2 levels in inflammatory exudate and with the influx of mononuclear inflammatory cells. Local administration of anti-inflammatory drugs such as dexamethasone, indomethacin, or a PLA2 inhibitor such as p-bromophenacyl bromide significantly inhibited exudate volume, cellular influx, granuloma formation, exudate PGE2 levels and PLA2 activity, to varying degrees. Dexamethasone treatment significantly reduced all parameters determined, whereas p-bromophenacyl bromide had a significant inhibitory effect on PLA2 activity and PGE2 release, and indomethacin only restored PGE2 levels. These results show that PLA2 is neither the only nor the most important factor involved in the development of subchronic inflammation.