Phospholipase A2 acyl-hydrolytic activity in rat RPAR-induced pleurisy.

Endogenous phospholipase A2 (PLA2) specific activity (SA) (% hydrolysis/min/mg protein) in the rat pleural cavity, measured as the acyl-hydrolysis of [3H]-arachidonic acid E. coli substrate, was quantitated after induction of a reverse passive Arthus reaction (RPAR). PLA2 SA, derived when the rate of hydrolysis was linear (1-5 min), was 1.9, 1.4, 3.8 and 4.1% h/min/mg at 10 min, 2 h, 4 h and 24 h, respectively, after induction of the RPAR. This time course appeared to correlate with the influx of mononuclear inflammatory cells, although the effect of plasma leakage on changes in exudate PLA2 SA could not be determined. Oral administration of antiinflammatory drugs significantly inhibited pleural fluid exudation and inflammatory cell influx to varying degrees. However, whereas these drugs additionally reduced total exudate protein and PLA2, they had no effect on the concentration of either parameter, implying that pleural PLA2 may be passively linked to fluid and cell movement.