Abstract
After peripheral injury and inflammation, the close relationship between stimulus intensity and response to acute injurious stimuli is altered. Peripheral injury and inflammation increase a subject’s responsiveness to noxious stimuli (i.e. pain reports, paw withdrawal latency, or electrophysiological recordings) relative to the un-injured state (Raja et al., 1988). This hypersensitivity can be expressed as a decreased response latency to a noxious stimulus (hyperalgesia) or a nocifensive response (i.e. pain report or escape attempts) to an innocuous stimulus (allodynia). These altered stimulus-response relationships may result from peripheral as well as central mechanisms; this review will focus on spinal prostanoid synthesis and hyperalgesia after peripheral injury and inflammation.
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Dirig, D.M., Yaksh, T.L. (1999). Spinal Synthesis and Release of Prostanoids After Peripheral Injury and Inflammation. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E.A. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 4. Advances in Experimental Medicine and Biology, vol 469. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4793-8_58
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DOI: https://doi.org/10.1007/978-1-4615-4793-8_58
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