The Arthus reaction in rats, a possible test for anti-inflammatory and antiheumatic drugs.

The Arthus reaction is an immunologically induced inflammatory response characterized by immune complex deposition, complement fixation, polymorphonuclear leukocyte infiltration and tissue damage. Many of these same pathological tissue alterations are found in the lesions of rheumatoid arthritis (RA). The similarities between the reversed passive Arthus reaction (RPAR) and RA led us to investigate the usefulness of the RPAR in the search for new antirheumatic agents. The RPAR was elicited in the skin of rats using chicken ovalbumin and the IgG fraction of rabbit anti-ovalbumin. Paramethasone, hydrocortisone, indomethacin, pirprofen, sulfinpyrazone, thalidomide and theophylline all gave significant inhibition of the RPAR. Ibuprofen, naproxen, cyprohepatadine and cromolyn sodium were inactive, while phenylbutazone and ASA exhibited a dose-dependent effect. The data show that the Arthus reaction, which is the result of the complex interaction of many factors, can be affected either generally or selectively at different time intervals by various therapeutic agents. The RPAR in rats may prove useful in detecting new therapeutic agents for the treatment of RA.

The effect of topically applied agents on ultraviolet erythema in guinea pigs.

It has been shown previously that ultraviolet erythema (UV) is partially the result of a local release of prostaglandins. We have studied the effects of different classes of pharmacological agents applied topically to the skin of guinea pigs and have found indomethacin and pirprofen, both prostaglandin synthetase inhibitors, to be highly effective suppressors of UV erythema. Our studies appear to further substantiate that prostaglandin synthesis and release may be the primary mechanistic process in the production of erythema and that the model itself can be predictive of both therapeutic and prophylactic effects of agents against sunburn.