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Cited by 57Pain Mechanisms and TreatmentsGastrointestinal motility and disordersIon Channels and Receptors

Peripheral contributions to visceral hyperalgesia.

Open access
Gebhart, GF·1999·Canadian Journal of Gastroenterology and Hepatology
DOI 10.1155/1999/730765
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Abstract

Hyperalgesia has long been recognized clinically as a consequence of tissue injury. Primary hyperalgesia (arising from the site of injury) is generally considered to be due to sensitization of sensory receptors (eg, nociceptors) and perhaps activation of so-called 'silent nociceptors' by mediators released, synthesized or attracted to the site of tissue injury. Key questions associated with understanding visceral hyperalgesia relate to whether the viscera are innervated by nociceptors (ie, sensory receptors that respond selectively to noxious intensities of stimulation), whether visceral receptors and/or afferent fibres sensitize after tissue injury and whether silent nociceptors exist in the viscera. Studies in nonhuman animals have revealed that hollow organs such as the esophagus, gall bladder, stomach, urinary bladder, colon and uterus are innervated by mechanically sensitive receptors with low or high thresholds for response. Accordingly, it appears that the viscera are innervated by nociceptors, although the issue is far from settled. One characteristic of cutaneous nociceptors is their ability to be sensitized when tissue is injured. Mechanosensitive visceral receptors also sensitize when the viscera are experimentally inflamed, but both visceral receptors with low thresholds and those with high thresholds for response are sensitized. Moreover, it is often not appreciated that visceral receptors are likely polymodal rather than unimodal - that is, mechanically sensitive visceral receptors typically are also sensitive to chemical and/or thermal stimuli. In this sense, visceral receptors may be considered evolutionarily older than more highly developed, specialized cutaneous receptors. Finally, there are mechanically insensitive receptors that innervate the viscera and, when tissue is injured, develop spontaneous activity and acquire sensitivity to mechanical stimuli. In the aggregrate, visceral receptors change their behaviour in the presence of tissue injury and, along with activated mechanically insensitive receptors, increase the afferent barrage into the spinal cord, contributing to the development of visceral hyperalgesia.

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  • Once activated, C-fibers can become sensitized, meaning they no longer remain silent even after inflammation resolves.

    “Once activated, C-fibers can become sensitized, meaning that they no longer remain silent even after inflammation resolves (Gebhart, 1999; Fig. 1, Part 1).”

    From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Gebhart, 1999

    The “Mechanically Insensitive Afferent Fibres” section says previously silent visceral fibres become spontaneously active and responsive to mechanical stimulation after experimental inflammation; Figure 6 (p. 40A) illustrates this change. The paper does not say they remain active after inflammation resolves, or identify these fibres specifically as C-fibres. (LLM, conf=0.86)

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  • Sprouting is known to be associated with an increase in the background and evoked activity of these fibers; fibers that develop sprouts become sensitized, which contributes to protein extravasation.

    “Such sprouting is known to be associated with an increase in the background and evoked activity of these fibers; that is, fibers that develop sprouts become sensitized [17], [18], which contributes to protein extravasation [13].”

    From Sprouted Innervation into Uterine Transplants Contributes to the Development of Hyperalgesia in a Rat Model of Endometriosis (2012) · cites this paper as [17]

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Research works printed but not linked: 4

  1. Mayer EM, Gebhart GF. Functional bowel disorders and visceral hyperalgesia. Gastroenterology 1994;107:271-93.
  2. Woolf CJ. Excitability changes in central neurons following peripheral damage. In: Willis WD, ed. Hyperalgesia and Allodynia. New York: Raven Press, 1992:221-43.
  3. Sengupta JN, Gebhart GF. Mechanosensitive afferent fibers in the gastrointestinal and lower urinary tracts. In: Gebhart GF, ed. Visceral Pain. Seattle: IASP Press, 1995:75-98.
  4. Sengupta JN, Su X, Gebhart GF. k, but not µ or s, opioids attenuate responses to distension of afferent fibers innervating the rat colon. Gastroenterology 1996;111:968-80.

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Authors
Gebhart, G.
Affiliations
University of Iowa (US)
Corresponding author
Gebhart, GF
Venue
Canadian Journal of Gastroenterology and Hepatology
Publisher
Wiley
Published
1999-01
Volume
13
Issue
A
Pages
37A-41A
ISSN
  • 2291-2789 (ISSN-L)
  • 2291-2797
DOI
10.1155/1999/730765
OpenAlex
W69388401
Cited by
57
References
14
Citations by year
2023: 4 · 2022: 2 · 2021: 2 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 2
FWCI
1.32
Type
journal article
Language
en
Open access
Licence
Locations
  • Canadian Journal of Gastroenterology and Hepatology (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Institutes of Health (NS 19912, DA 02897)
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
visceral hypersensitivity, nociceptors, visceral afferents, receptor sensitization, tissue damage, visceral inflammation, polymodal receptors, visceral pain
MeSH terms
Animals, Humans, Hyperalgesia, Intestines, Mechanoreceptors, Nerve Fibers, Nociceptors, Pain

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