Altered sympathovagal balance and pain hypersensitivity in TNBS-induced colitis

• Published in: Archives of medical science Vol. 13; no. 1; pp. 246 - 255
• Main Authors: Ciesielczyk, Katarzyna, Furgała, Agata, Dobrek, Łukasz, Juszczak, Kajetan, Thor, Piotr
• Format: Journal Article
• Language: English
• Published: Poland Termedia Publishing House 01.02.2017
• Subjects: colitis; Experimental Research; heart rate variability; inflammatory bowel disease; pain hypersensitivity; colitis; heart rate variability; pain hypersensitivity; inflammatory bowel disease
• ISSN: 1734-1922; 1896-9151
• DOI: 10.5114/aoms.2015.55147

Pain hypersensitivity, abnormal motility and autonomic dysfunction contribute to functional symptoms of inflammatory bowel disease (IBD). 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. Experimental colitis resulted in a significant decrease in pain threshold (MA 23.60 ±2.12, < 0.001, TH 8.51 ±1.49, < 0.001), reduced expulsion time (6.2 ±3.5, < 0,01) and increase in the sympathetic autonomic activity (LFnu 32.54 ±21.16, < 0.03). The animals with diminished vagal integrity presented with reduced gastrointestinal motility (39.8 ±25.1, < 0.01) and a decrease in the parasympathetic high-frequency domain of HRV (HFnu 55.37 ±22.80, < 0.002). The vagotomized rats with colitis showed the strongest nociceptive response (MA 22.46 ±3.02, < 0.004; TH 7.99 ±1.12, < 0.003) as well as significant changes in sympatho-vagal balance on HRV testing (LFnu 28.25 ±14.66, < 0.04; HFnu 71.34 ±14.55, < 0.04). 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.