hyperalgesia

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hyperalgesia

[¦hī·pər·al′jē·zhə]
(physiology)
Increased or heightened sensitivity to pain stimulation.
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Repeated intradermal administration of the potent and highly selective mu-opioid agonist, [d-Ala(2),N-MePhe(4),gly-ol]-enkephalin, to produce tolerance due to its inhibition of prostaglandin E(2) hyperalgesia, simultaneously produced hyperalgesic priming.
Hyperalgesic priming is restricted to isolectin B4-positive nociceptors.
Furthermore, M40403 was found to inhibit a central hyperalgesic response by preventing nitration and subsequent deactivation of endogenous spinal superoxide dismutase, the enzyme that normally lowers the levels of superoxide.
This key finding supports the concept that nitration and subsequent inactivation of endogenous spinal superoxide dismutase is a critical event in the hyperalgesic response, possibly by allowing the levels of superoxide to remain elevated and in turn maintain nociceptive signaling.
The tantalising possibility exists that exposure to buprenorphine, possibly in quite low doses, in combination with other opioid and analgesic drugs, will improve pain relief, by reducing putative hyperalgesic and pronociceptive effects.
Administration of diclofenac, HLEE or diclofenac-HLEE combination, but not vehicles, produced a reduction in the hyperalgesic effect induced by carrageenan (p<0.
In our study, systemic administration of HLEE was able to decrease the hyperalgesic effect induced by carrageenan in the mouse.