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Nitric oxide and inflammatory pain

  • Chapter
Pain and Neurogenic Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

Inflammation in the periphery often leads to pathological pain processes such as allodynia (reduction in pain threshold), hyperalgesia (increased response to noxious stimuli), persistent pain (increase in the duration of the response to a brief stimulation) and secondary hyperalgesia (a spread of pain and hyperalgesia to non-inflamed tissue). Increased pain in response to stimulation during inflammation depends on both an increase in sensitivity of primary afferent nociceptors at the site of inflammation and an increase in the excitability of neurones in the central nervous system (CNS; i.e. peripheral and central sensitisation respectively). The following chapter discusses the probable role of nitric oxide (NO) in both peripheral, and especially, central sensitisation evoked by an inflammatory response. A brief overview of NO synthesis, biological effects and isoforms is provided in order to examine the extent of NO mediated pathophysiological responses during inflammatory pain.

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Handy, R.L.C. (1999). Nitric oxide and inflammatory pain. In: Brain, S.D., Moore, P.K. (eds) Pain and Neurogenic Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8753-3_5

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  • DOI: https://doi.org/10.1007/978-3-0348-8753-3_5

  • Publisher Name: Birkhäuser, Basel

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