Articles: hyperalgesia.
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Drug combinations have the potential advantage of greater analgesia over monotherapy. The present study was aimed to assess any possible interaction (additive or potentiation) in the antinociceptive effects of etoricoxib; a novel cyclooxygenase-2 inhibitor, and tramadol; a typical opioid agonist when administered in combination against mechanical hyperalgesia induced by spinal cord injury in rats. The nature of interaction was analyzed using surface of synergistic interaction (SSI) analysis and an isobolographic analysis. ⋯ The SSI was calculated from the total antihyperalgesic effect produced by the combination after the subtraction of the antihyperalgesic effect produced by each of the individual drug. In the isobolographic analysis, the experimental ED50 was found to be far below the line of additivity also indicating a significant (P < 0.05) synergistic antihyperalgesic effect when etoricoxib and tramadol was co-administered to rats. The synergistic antihyperalgesic effect of etoricoxib and tramadol combination suggests that these combinations may have clinical utility in mechanical hyperalgesia associated with spinal injury.
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Opioid analgesics are effective for treating many pain conditions. Opioid analgesic tolerance is a pharmacologic phenomenon that could affect the clinical use of opioid analgesics. ⋯ Thus, exposure to opioids could lead to two seemingly unrelated cellular processes (ie, the development of opioid tolerance and opioid-induced pain sensitivity). Their converging effects may be part of the mechanisms leading to the reduced opioid analgesic efficacy in chronic opioid therapy.
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Comparative Study
The opioid peptide nociceptin/orphanin FQ mediates prostaglandin E2-induced allodynia, tactile pain associated with nerve injury.
Pain often outlasts its usefulness as warning and aid in wound healing, and becomes chronic and intractable after tissue damage and nerve injury. Many molecules have been implicated as mediators and modulators in persistent pain such as hyperalgesia and tactile pain (allodynia). We previously showed that prostaglandin (PG) E(2), PGF(2alpha) or the neuropeptide nociceptin, also called orphanin FQ (N/OFQ) administered intrathecally (i.t.) produced allodynia in conscious mice. ⋯ Conversely, PGE(2)-induced allodynia was not observed in ppN/OFQ(-/-) mice. N/OFQ immunoreactive puncta were colocalized with EP4. Taken together, these results demonstrate that PGE(2) induced allodynia by stimulation of N/OFQ release in the spinal cord via EP4 receptor subtypes.
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Melittin, which is a principal protein of honeybee venom, can induce mechanical hyperalgesia in humans. The characteristics of the melittin induced mechanical hyperalgesia are quantitatively and qualitatively different from those evoked by capsaicin. The aim of the present study was to investigate in detail secondary heat hyperalgesia induced by melittin in humans. ⋯ The pain rating index at 60 min was significantly larger than at 5 min (P=0.04) and at 30 min (P=0.03). These results demonstrated slowly developing secondary heat hyperalgesia after injection of melittin. A possible contribution of peripheral inflammatory responses to the manifestation of secondary heat hyperalgesia is suggested, which in reality render the distinction between the primary and secondary area of heat hyperalgesia unnecessary.
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Wien. Klin. Wochenschr. · Feb 2006
Controlled Clinical TrialHyperalgesia against capsaicin in persons with un-investigated dyspepsia: potential as a new diagnostic test.
Lack of understanding of the pathogenesis of functional dyspepsia is one reason for the paucity of effective treatment options. Whereas mechanical sensitivity in persons suffering from dyspepsia might be impaired, chemically induced hypersensitivity has received little attention. The aim of this study was to evaluate whether vanilloid receptors stimulated by capsaicin are hypersensitive in persons with dyspepsia. ⋯ Jejunal sensitivity to capsaicin is increased in persons with un-investigated dyspepsia, and vanilloid receptors might be involved in the pathophysiology of this condition. Patients with hypersensitivity to chemical stimuli may represent a distinct subpopulation based on the underlying pathophysiology and may require specific treatment to restore normal visceral sensitivity.