Hypotheses on a possible role of some mediators in various inflammatory reactions on mouse ear.

Thanks to local application of various compounds that inhibit the effects or the synthesis of histamine, serotonin, prostaglandins, thromboxanes and leukotrienes, hypotheses are proposed about the possible role of these mediators in various experimental inflammations induced on mouse ear: reactions to arachidonic acid, croton oil and cantharidin (6-h and 24-h phases); primary irritation and delayed hypersensitivity reaction to picryl chloride; and semi-delayed (6-h) and delayed (24-h) hypersensitivity to oxazolone. Histamine seems to play a major role in the acute phase (6-h) of the reaction to cantharidin and in the primary irritation due to picryl chloride. Serotonin seems to be more involved in edema due to arachidonic acid and to croton oil and in the semi-delayed phase of hypersensitivity to oxazolone. Leukotrienes seem to have a more pronounced role in arachidonic-acid-induced inflammation and in the primary irritation and delayed hypersensitivity reactions to picryl chloride. Prostaglandins and/or thromboxanes might have some influence in edema due to arachidonic acid and to croton oil, and in the primary irritation reaction to picryl chloride.