Oxygen-derived free radicals mediate the cutaneous necrotizing vasculitis induced by epinephrine in endotoxin-primed rabbits.

Abstract

To assess the possible role of oxygen-derived free radical in the pathogenesis of cutaneous necrotizing vasculitis (Thomas reaction) induced by epinephrine in endotoxin-primed rabbits, animals were treated with superoxide dismutase (intraperitoneal or local), catalase, allopurinol, or ibuprofen 2 h before inducing the reaction. This is done by an earlobe intravenous injection (10 micrograms) of endotoxin followed by an intradermal injection (100 micrograms) of epinephrine in the shaved abdomen; 18-24 h later, a hemorrhagic-necrotic lesion can be observed at the site of the epinephrine injection. The reaction was completely inhibited by superoxide dismutase, catalase, and ibuprofen, while allopurinol afforded only partial protection. Thus, oxyradicals seem to participate in the pathogenesis of this reaction.