A comparison of hyperalgesia and neurogenic inflammation induced by melittin and capsaicin in humans

Melittin (a main compound of bee venom) and capsaicin were injected intradermally in healthy human volunteers: (1) to study secondary mechanical hyperalgesia (static hyperalgesia and dynamic hyperalgesia) around the injection site; and (2) to correlate the sensory changes to the neurogenic inflammat...

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Bibliographic Details
Published in:Neuroscience letters 2003-02, Vol.337 (3), p.147-150
Main Authors: Sumikura, H., Andersen, O.K., Drewes, A.M., Arendt-Nielsen, L.
Format: Article
Language:English
Subjects:
Analysis of Variance
Bee venom test
Bee Venoms - adverse effects
Capsaicin
Capsaicin - adverse effects
Flare
Humans
Hyperalgesia - chemically induced
Hyperalgesia - physiopathology
Injections, Intradermal
Melitten - adverse effects
Melittin
Neurogenic inflammation
Neurogenic Inflammation - chemically induced
Neurogenic Inflammation - physiopathology
Pain - etiology
Pain Measurement - drug effects
Physical Stimulation
Regional Blood Flow - drug effects
Secondary hyperalgesia
Skin - blood supply
Time Factors
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Summary:Melittin (a main compound of bee venom) and capsaicin were injected intradermally in healthy human volunteers: (1) to study secondary mechanical hyperalgesia (static hyperalgesia and dynamic hyperalgesia) around the injection site; and (2) to correlate the sensory changes to the neurogenic inflammation assessed by laser-doppler blood flowmetry. Melittin 50 μg and capsaicin 10 μg induced comparable spontaneous pain and increased blood flow (neurogenic inflammation). Intradermal injection of melittin induced regions of secondary mechanical hyperalgesia around the injection site, however, they were not as large as the hyperalgesia induced by capsaicin. This is the first report studying mechanical hyperalgesia induced by melittin in humans, and the results were in agreement with the previous observations in rats. Melittin seems to be a valuable model to study a possible contribution of neurogenic inflammation to hyperalgesia in humans.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(02)01325-3