Articles: hyperalgesia.
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Randomized Controlled Trial
[Modulation of cortical pain processing by cyclooxygenase inhibition: a functional MRI study].
Little is known about changes in brain activity with pharmacological modulation of hyperalgesia. Therefore, we sought to investigate the cerebral processing of hyperalgesia and acute pain using functional magnetic resonance imaging (fMRI) and pharmacological modulation with cyclooxygenase (COX) inhibitors. ⋯ This study provides new evidence for the involvement of COX inhibitors in modulating the cerebral activity associated with acute pain and hyperalgesia. Our results hint at a differential modulation of brain areas under either analgesia or antihyperalgesia.
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Anesthesia and analgesia · Apr 2009
Antiinflammatory and antihyperalgesic activity of C-phycocyanin.
C-phycocyanin (C-PC), a biliprotein found in blue green algae, such as Spirulina platensis, is often used as a dietary nutritional supplement due to its various therapeutic values. In addition, the antiinflammatory activity of C-PC partly through inhibition of proinflammatory cytokine formation, inducible nitric oxide synthase (iNOS) and cyclooxygeanase-2 (COX-2) expression has been demonstrated in many in vitro and in vivo studies. However, whether C-PC also has antihyperalgesic activity in inflammatory nociception has not been investigated. ⋯ Based on these results, it is suggested that the inhibition of NO and prostaglandin E(2) over-production through suppressing iNOS and COX-2 induction and attenuation of TNF-alpha formation and neutrophil infiltration into inflammatory sites by C-PC may contribute, at least in part, to its antihyperalgesic activity.
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Endothelins, acting through specific endothelin ET(A) and/or ET(B) receptors, participate in nociceptive processing in models of cancer, inflammatory and neuropathic pain. The present study investigated which cell types express endothelin receptors in the trigeminal ganglion, and the contribution of mechanisms mediated by endothelin ET(A) and ET(B) receptors to orofacial heat hyperalgesia induced by unilateral constriction of the infraorbital nerve (CION). Both receptor types were identified by immunohistochemistry in the trigeminal ganglion, ET(A) receptors on small-sized non-myelinated and myelinated A-fibers and ET(B) receptors on both satellite glial cells and small-sized non-myelinated neuronal cells. ⋯ On the other hand, CION-induced heat hyperalgesia was transiently abolished over the first 90 min following i.p. injection of morphine hydrochloride (2.5 mg/kg), but fully resistant to reversal by indomethacin (4 mg/kg, i.p.) or celecoxib (10 mg/kg, i.p.). Thus, heat hyperalgesia induced by CION is maintained, in part, by peripheral signaling mechanisms operated by ET(A) and ET(B) receptors. Endothelin receptors might represent promising therapeutic targets for the control of trigeminal neuropathic pain.
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Experimental glutamate and capsaicin-induced pain has not been described in tendon tissue despite the implications of addressing these receptors in pain management strategies. This study investigated pain induction and modulatory interactions by injecting glutamate (0.5 ml, 1 M) and capsaicin (0.5 ml, 5 microg, 33 microM) to human tendon tissue. Following the initial glutamate or capsaicin injection, a second injection of either glutamate (following capsaicin), capsaicin (following glutamate) or hypertonic saline (after both glutamate and capsaicin) was given. ⋯ The results indicate in tendon tissue a facilitation of response to capsaicin injection following glutamate injection. PPTs were only reliably reduced by capsaicin injection. These results emphasize the possible importance of peripheral glutamate receptor antagonists in pain management in musculoskeletal conditions.
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TNFalpha plays a pivotal role in rheumatoid arthritis (RA) but little is known of the mechanisms that link the inflammatory and nociceptive effects of TNFalpha. We have established a murine model of TNFalpha-induced TRPV1-dependent bilateral thermal hyperalgesia that then allowed us to identify distinct peripheral mechanisms involved in mediating TNFalpha-induced ipsilateral and contralateral hyperalgesia. Thermal hyperalgesia and inflammation were assessed in both hindpaws following unilateral intraplantar (i.pl.) TNFalpha. ⋯ However, TNFalpha-induced IL-1beta generation in both paws and the presence of local IL-1beta in the contralateral paw were essential for the development of bilateral hyperalgesia. These results identify a series of peripheral events through which TNFalpha triggers and maintains bilateral inflammatory pain. This potentially allows a better understanding of mechanisms involved in TNFalpha-dependent pain pathways in symmetrical diseases such as arthritis.