A study of chemically induced acute inflammation in the skin of the rat

Oedema due to application of benzene to the skin was reduced following prior sensory denervation and in animals systemically pre-treated with capsaicine (which is known to confer resistance to chemical irritants) or compound 48/80 (which depletes the body of mast cells). Increased degranulation of mast cells in the benzene-treated skin was unaffected by denervation but did not occur after treatment with capsaicine. Antidromic stimulation of a cutaneous nerve caused oedema and degranulation of mast cells, both of which were less severe than the corresponding effects of topically applied benzene. These effects were completely prevented by prior treatment with capsaicine and the oedema was less severe in 48/80-treated rats. Hence, the presence of mast cells was necessary for full development of the effects of antidromic stimulation. These observations indicate that axon reflexes in sensory fibres contribute to, but are not entirely responsible for, the development of oedema in chemically irritated skin. The prophylactic action of capsaicine may be due to the prevention of degranulation of mast cells rather than to a direct effect on cutaneous nerve endings. These conclusions are embodied in an hypothesis purporting to explain the involvement of axon reflexes, mast cells and various humoral mediators in chemically induced acute inflammation.