A model of Arthus pleurisy: modulation by various pharmacologic and therapeutic agents.

A reversed passive Arthus reaction was elicited in the rat pleural cavity. The kinetics of this inflammatory response indicate that exudate volume (cells and fluid) reaches a maximum level approximately 2 to 4 hr postantibody challenge. The neutrophil is the major cellular constituent of the pleural exudate during the first 12 hr of this reaction, reaching peak values at 4 hr; whereas, the monocyte predominates between 15 and 24 hr. Lymphocytes, eosinophils, and mast cells were also identified in the pleural exudates. The serotonin antagonists, cyproheptadine and methylsergide, and the antihistamine, chlorpheniramine, demonstrated marginal activity in the Arthus pleurisy model. The histamine antagonist, metiamide, was inactive. The nonsteroidal anti-inflammatory agents, flurbiprofen, ibuprofen, indomethacin, and benoxaprofen caused a modest suppression of exudate volume (18-32%) and cell accumulation (28-34%). The fluid and cellular components of the Arthus reaction were significantly inhibited by dexamethasone, triamcinolone, paramethasone, and prednisolone. The oral gold preparation, auranofin, had a pronounced effect on exudate volume; whereas, other antirheumatic agents such as D-penicillamine, azathioprine, and chloroquine had no effect on the Arthus pleurisy reaction. The immunomodulator, levamisole, suppressed exudate volume, but had no effect on cell accumulation in the pleural cavity.