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Peripheral contributions to visceral hyperalgesia.

G F Gebhart1

  • 1Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa 52242-1109, USA. gf-gebhart@uiowa.edu

Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie
|April 15, 1999
PubMed
Summary

Visceral hyperalgesia results from tissue injury causing sensitization of visceral receptors and activation of mechanically insensitive afferents. These changes increase nerve signals to the spinal cord, leading to heightened pain sensitivity.

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Area of Science:

  • Neuroscience
  • Pain Research
  • Gastroenterology

Background:

  • Hyperalgesia, or increased pain sensitivity, is a known outcome of tissue injury.
  • Understanding visceral hyperalgesia requires investigating visceral innervation, receptor sensitization, and the presence of silent nociceptors.

Purpose of the Study:

  • To explore the innervation of viscera by nociceptors.
  • To determine if visceral receptors and afferent fibers sensitize after injury.
  • To investigate the existence and role of silent nociceptors in visceral pain.

Main Methods:

  • Review of studies on nonhuman animal models examining visceral organ innervation.
  • Analysis of experimental data on visceral inflammation and receptor responses.
  • Examination of the characteristics of visceral afferent fibers, including mechanosensitivity and polymodality.

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Main Results:

  • Hollow visceral organs are innervated by mechanosensitive receptors with varying thresholds, suggesting the presence of nociceptors.
  • Both low- and high-threshold mechanosensitive visceral receptors sensitize during inflammation.
  • Visceral receptors are often polymodal, responding to mechanical, chemical, and thermal stimuli.
  • Mechanically insensitive afferents in the viscera become active and sensitive to mechanical stimuli following injury.

Conclusions:

  • Evidence supports the innervation of viscera by nociceptors, though further research is needed.
  • Visceral tissue injury induces sensitization of existing receptors and activation of previously insensitive ones.
  • These neuroplastic changes in visceral afferents contribute significantly to the development of visceral hyperalgesia.