Details

Autor(en) / Beteiligte

• Gil, D. W.
• Wang, J.
• Gu, C.
• Donello, J. E.
• Cabrera, S.
• Al‐Chaer, E. D.

Titel

Role of sympathetic nervous system in rat model of chronic visceral pain

Ist Teil von

• Neurogastroenterology and motility, 2016-03, Vol.28 (3), p.423-431

Ort / Verlag

England: Wiley Subscription Services, Inc

Erscheinungsjahr

2016

Quelle

Wiley-Blackwell Journals

Beschreibungen/Notizen

• Background Changes in central pain modulation have been implicated in generalized pain syndromes such as irritable bowel syndrome (IBS). We have previously demonstrated that reduced descending inhibition unveils a role of sympathoneuronal outflow in decreasing peripheral sensory thresholds, resulting in stress‐induced hyperalgesia. We investigated whether sympathetic nervous system (SNS) exacerbation of pain sensation when central pain inhibition is reduced is relevant to chronic pain disorders using a rat colon irritation (CI) model of chronic visceral hypersensitivity with hallmarks of IBS. Methods Rats were treated to a series of colorectal balloon distensions (CRD) as neonates resulting in visceral and somatic hypersensitivity and altered stool function that persists into adulthood. The visceral sensitivity was assessed by recording electromyographic (EMG) responses to CRD. Somatic sensitivity was assessed by paw withdrawal thresholds to radiant heat. The effects on the hypersensitivity of (i) inhibiting sympathoneuronal outflow with pharmacological and surgical interventions and (ii) enhancing the outflow with water avoidance stress (WAS) were tested. Key Results The alpha2‐adrenergic agonist, clonidine, and the alpha1‐adrenergic antagonist, prazosin, reduced the visceral hypersensitivity and WAS enhanced the pain. Chemical sympathectomy with guanethidine and surgical sympathectomy resulted in a loss of the chronic visceral hypersensitivity. Conclusions & Inferences The results support a role of the SNS in driving the chronic visceral and somatic hypersensitivity seen in CI rats. The findings further suggest that treatments that decrease sympathetic outflow or block activation of adrenergic receptors on sensory nerves could be beneficial in the treatment of generalized pain syndromes. This study examines the role of sympathetic outflow in chronic visceral hypersensitivity using recordings of electromyographic responses to colorectal distension in a rat colon irritation (CI) model with hallmarks of irritable bowel syndrome (IBS). Clonidine — alpha2‐adrenergic agonist — and prazosin — alpha1‐adrenergic antagonist—reduced the visceral hypersensitivity. Chemical sympathectomy with guanethidine and surgical sympathectomy also resulted in a loss of the chronic visceral hypersensitivity. The results support a role of the sympathetic nervous system in driving the chronic visceral and somatic hypersensitivity seen in CI rats. They further suggest that treatments that decrease sympathetic outflow or block activation of adrenergic receptors on sensory nerves could be beneficial in the treatment of generalized pain syndromes such as IBS. The sympathetic nervous system (SNS) exacerbates pain sensation when central pain inhibition is reduced; this observation is highly relevant to chronic pain disorders. View the podcast on this paper at the following sites: iTunes: https://itunes.apple.com/gb/podcast/neurogastroenterology-motility/id1082302537 Youtube: https://www.youtube.com/watch?v=yZBC4lZ4JVY&feature=youtu.be