The effect of cutaneous mast cell degranulation on sensitivity to heat

  • Drummond P
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Abstract

OBJECTIVE: To determine whether depletion of inflammatory mediators from cutaneous mast cells influences cutaneous sensitivity to heat or the thermal hyperalgesia provoked by capsaicin or noradrenaline.

SUBJECTS: Ten healthy men.

METHODS AND RESULTS: Compound 48/80 was introduced by iontophoresis into the forearm. Wheals at the site of compound 48/80 iontophoresis subsided over four pre-treatments, consistent with mast cell degranulation. Flares in the skin surrounding the compound 48/80 sites decreased after the first pre-treatment but persisted to some extent after wheals had disappeared, suggesting that a reagent produced during mast cell activation (e.g., a cytokine or lipoxygenase product released from degranulated mast cells) triggered a residual flare. Sensitivity to heat increased after the second administration of compound 48/80, possibly due to sensitization of thermal nociceptors by inflammatory mediators released from infiltrating leukocytes. However, the compound 48/80 pre-treatment inhibited the hyperalgesic effect of capsaicin. Pre-treatment with compound 48/80 did not prevent axon-reflex vasodilatation to noradrenaline or the hyperalgesic effect of noradrenaline in capsaicin-treated skin.

CONCLUSIONS: Two mechanisms could account for the inhibitory effect of the compound 48/80 pre-treatment on the hyperalgesic effect of capsaicin. First, mast cell products could partly mediate the hyperalgesic effect of capsaicin. Second, partial desensitization of the vanilloid receptor subtype-1 by a reagent produced during mast cell activation (e.g., a lipoxygenase product) could mask the hyperalgesic effect of capsaicin. Mast cells do not appear to mediate the hyperalgesic effect of noradrenaline.

Author-supplied keywords

  • Axon-reflex
  • Capsaicin
  • Mast cells
  • Noradrenaline
  • Thermal hyperalgesia

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Authors

  • P. D. Drummond

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