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Non-steroidal Anti-inflammatory Drugs and Pain

  • Chapter
The Pharmacology of Pain

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 130))

Abstract

During inflammation numerous events occur resulting in nociception of peripheral stimuli. Inflammatory cells and peripheral nerves release a variety of mediators including Prostaglandins (PGs). This results in a change of high-threshold mechanoceptors into nociceptors. Changes in the central nervous system (CNS) also occur. This is particularly evident in the dorsal horn of the spinal cord where reflex and metabolic activity of neuronal cells is increased. Collectively these events result in hyperalgesia. Traditionally it was believed that non-steroidal anti-inflammatory drugs (NSAIDs) reduce the enhanced nociceptor activity in the periphery by inhibition of the sensitising effects of PGs. This is based on the finding that all of the hyperalgesic eicosanoids induce cyclic adenosine monophosphate, which in turn mediates the peripheral hyperalgesia of primary afferent nociceptors (Taiwo et al. 1989). However, as is discussed below, numerous other analgesic mechanisms of action separate from inhibition of PG formation are now attributed to NSAIDs.

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© 1997 Springer-Verlag Berlin Heidelberg

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Appleton, I. (1997). Non-steroidal Anti-inflammatory Drugs and Pain. In: Dickenson, A., Besson, JM. (eds) The Pharmacology of Pain. Handbook of Experimental Pharmacology, vol 130. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60777-6_3

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  • DOI: https://doi.org/10.1007/978-3-642-60777-6_3

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