Altered sympathovagal balance and pain hypersensitivity in TNBS-induced colitis

doi:10.5114/aoms.2015.55147

Altered sympathovagal balance and pain hypersensitivity in TNBS-induced colitis

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Altered sympathovagal balance and pain hypersensitivity in TNBS-induced colitis

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punktacja MEiN [2017 A]: 30

title:	Altered sympathovagal balance and pain hypersensitivity in TNBS-induced colitis
author:	Ciesielczyk Katarzyna , Furgała Agata , Dobrek Łukasz , Juszczak Kajetan , Thor Piotr
journal title:	Archives of Medical Science
volume:	13
issue:	1
date of publication :	2017
pages:	246-255
ISSN:	1734-1922
eISSN:	1896-9151
DOI:	10.5114/aoms.2015.55147
language:	English
journal language:	English
abstract in English:	Introduction: Pain hypersensitivity, abnormal motility and autonomic dysfunction contribute to functional symptoms of inflammatory bowel disease (IBD). Material and methods: The aim of this study was to assess: nociceptive thresholds for mechanical allodynia (MA) and thermal hyperalgesia (TH), intestinal motility (distal colonic transit and emptying), and cardiac autonomic neuropathy (indices of heart rate variability – HRV) in male Wistar rats with experimental trinitrobenzene sulfonic acid (TNBS) induced colitis. To identify a potential vagal contribution the bilateral subdiaphragmatic vagotomy (SDV) was performed. Results: Experimental colitis resulted in a significant decrease in pain threshold (MA 23.60 ±2.12, p < 0.001, TH 8.51 ±1.49, p < 0.001), reduced expulsion time (6.2 ±3.5, p < 0,01) and increase in the sympathetic autonomic activity (LFnu 32.54 ±21.16, p < 0.03). The animals with diminished vagal integrity presented with reduced gastrointestinal motility (39.8 ±25.1, p < 0.01) and a decrease in the parasympathetic high-frequency domain of HRV (HFnu 55.37 ±22.80, p < 0.002). The vagotomized rats with colitis showed the strongest nociceptive response (MA 22.46 ±3.02, p < 0.004; TH 7.99 ±1.12, p < 0.003) as well as significant changes in sympatho-vagal balance on HRV testing (LFnu 28.25 ±14.66, p < 0.04; HFnu 71.34 ±14.55, p < 0.04). Conclusions: The relationship between the cardiovascular and gastrointestinal system is modulated by neural, hormonal and inflammatory factors. This leads to dysregulation of the brain-gut interactions in the course of IBD. Sensitization and visceral-somatic convergence trigger pain hypersensitivity and autonomic sympathovagal imbalance. While integral vagal innervation impacts analgesic mechanisms via modulation of the immune response, SDV raises sympathetic activity and induces excessive hyperalgesia.
keywords in English:	inflammatory bowel disease, colitis, pain hypersensitivity, heart rate variability
departmental parameterization:	30
affiliation:	Wydział Lekarski : Zakład Patofizjologii
type:	journal article
subtype:	academic paper

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