Modulation by various locally applied anti-inflammatory and anti-allergic compounds of the immune and non-immune inflammation induced by picryl chloride in mice.

The authors studied the primary irritation and contact delayed hypersensitivity inflammation induced by picryl chloride in mice. The primary irritation reaction was induced by the application of various concentrations of the phlogogenic agent on an ear. Seven days after contact sensitization of the animals on their shaved abdomen, the immune inflammation was also induced on an ear by various doses of picryl chloride. Clear 24 hour-delayed hypersensitivity reactions were induced only by picryl chloride doses that induced a primary oedematous irritation 3 to 6 hours after application. After selection of the 3%-concentration of picryl chloride for challenge on ear, attempts were made to modulate these two types of reaction pharmacologically with various anti-allergic or anti-inflammatory compounds mixed with the inflammation-inducing agent. The inhibition of the non-immune reaction by mepyramine, methysergide, and the two anti-allergic compounds F 1865 and disodium cromoglycate demonstrated the participation of histamine and serotonin in this inflammation. Vasoactive amines seemed also to be involved in the immune reaction, but to a lesser extent. Hydrocortisone reduced the two types of inflammation by the same amount, while desonide had more effect on the delayed hypersensitivity reaction. In addition, both indomethacin and acetylsalicylic acid affected the two reactions equally, whereas phenylbutazone had a greater effect on the primary irritation inflammation.