title: Effect of change in an inhibitory neurotransmitter of the myenteric plexus on the pathogenetic mechanism of irritable bowel syndrome subgroups in rat models.
abstract: OBJECTIVE
  In order to investigate the effect of change in an inhibitory neurotransmitter of the myenteric plexus on irritable bowel syndrome (IBS) subgroups, the amounts of nitric oxide (NO) in constipation-predominant (C-IBS) and diarrhea-predominant (D-IBS) IBS models in rats were studied.
  
  
  METHODS
  The D-IBS model was created in rats by intracolonic instillation of acetic acid and by restraint stress. The D-IBS control group underwent intracolonic instillation with saline instead. The C-IBS model was created in rats by gastric instillation of 0-4 degrees C cool water daily for 14 days. The C-IBS control group underwent gastric instillation with saline instead. A blank control group was also made. Viscerosomatic sensitivity was assessed with electromyographic (EMG). Abdominal contractions induced by distension of a colonically inserted balloon (0-1.6 mL) was recorded in rats by implanting electrodes in the abdominal external oblique muscle. An India ink gastric instillation experiment was used to detect the bowel movement and fecal pellets formation. Histological analysis of colonic tissue was performed. Nicotinamide dinucleotide phosphate (NADPH)-diaphorase staining was used to detect positive NO neurons in the myenteric plexus.
  
  
  RESULTS
  When the balloon was distended by high volume, there were significantly more contractions of abdominal muscle in D-IBS compared with C-IBS and the control groups (P < 0.05). When the balloon was distended by low volume, there were significantly fewer contractions of abdominal muscle in C-IBS compared with D-IBS and the control groups (P < 0.05). The wet weight and water content of the feces expelled by the rats in the C-IBS and the C-IBS control groups were significantly lower than those in the blank control group (P < 0.05). The time before the first black stool in the C-IBS group was significantly longer than that in the blank control group and C-IBS control group (P < 0.05). Histological analysis of the colon showed no colonic inflammation in any group. The number of NO-positive neurons in the C-IBS group was significantly greater than in the D-IBS and control groups (P < 0.01), although there was no significant difference in the number of neurons between the D-IBS and the control groups (P > 0.05).
  
  
  CONCLUSIONS
  Enhanced inhibitory neurotransmitter NO in the myenteric plexus of the colon is related to IBS subgroups, visceral sensitivity and motility dysfunction. The results reveal that NO plays a role in the pathogenetic mechanism of IBS subgroups.
authors.affiliation: Department of Gastroenterology, Second Hospital of Xi'an Jiaotong University, Shaanxi Province, China.
authors.forename: Jun Rong
authors.initials: JR
authors.lastname: Xu
authors.forename: Jin Yan
authors.initials: JY
authors.lastname: Luo
authors.forename: Lei
authors.initials: L
authors.lastname: Shang
authors.forename: Wu Ming
authors.initials: WM
authors.lastname: Kong
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002244:Carbon; D003248:Constipation / Q000473:pathology / Q000503:physiopathology; D003672:Defecation; D003967:Diarrhea / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005243:Feces / Q000737:chemistry; D005769:Gastrointestinal Motility; D043183:Irritable Bowel Syndrome / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D009197:Myenteric Plexus / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D009252:NADPH Dehydrogenase / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012007:Rectum / Q000378:metabolism / Q000473:pathology; D012149:Restraint, Physical
chemical_list: D015415:Biomarkers; D018377:Neurotransmitter Agents; C028433:chinese ink; D009569:Nitric Oxide; D002244:Carbon; D009252:NADPH Dehydrogenase