Authors: La JH, Kim TW, Sung TS, Kang JW, Kim HJ, Yang IS.
Institution: Department of Physiology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Aim: Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by visceral hypersensitivity and altered bowel motility. There is increasing evidence suggesting the role of inflammation in the pathogenesis of IBS, which addresses the possibility that formerly established rat model of colitis could be used as an IBS model after the inflammation subsided.Methods: Colitis was induced by intracolonic instillation of 4% acetic acid in male Sprague-Dawley rats. The extent of inflammation was assessed by histological examination and myeloperoxidase (MPO) activity assay. After subsidence of colitis, the rats were subjected to rectal distension and restraint stress, then the abdominal withdrawal reflex and the number of stress-induced fecal output were measured, respectively.
Results: At 2 days post-induction of colitis, the colon showed characteristic inflammatory changes in histology and 8-fold increase in MPO activity. At 7 days post-induction of colitis, the histological features and MPO activity returned to normal. The rats at 7 days post-induction of colitis showed hypersensitive response to rectal distension without an accompanying change in rectal compliance, and defecated more stools than control animals when under stress.
Conclusion: These results concur largely with the characteristic features of IBS, visceral hypersensitivity and altered defecation pattern in the absence of detectable disease, suggesting that this animal model is a methodologically convenient and useful model for studying a subset of IBS.
Related Studies:
- Effect of Transient Chemically Induced Colitis on the Visceromotor Response to Mechanical Colorectal Distension
- Experimental Colitis Alters Myenteric Nerve Function at Inflamed and Noninflamed Sites in the Rat
- Damage to the Enteric Nervous System in Experimental Colitis
- Previous Inflammation Alters the Response of the Rat Colon to Stress
