title: Experimental oesophagitis in the rat is associated with decreased voluntary movement.
abstract: Growing interest has arisen regarding the mechanism of dyspeptic symptom generation. However, no evaluation system of these symptoms in animals has been developed. In this study, we examined whether voluntary movement of rats could be a measure to assess visceral symptoms of reflux oesophagitis. A chronic acid reflux oesophagitis model was made using rats, and the size of erosions was measured. Omeprazole was administered to the oesophagitis rats for 10 days. The amount of voluntary movement was measured by an infrared sensor. Intracellular spaces in oesophageal epithelium were also measured using a emission electron microscope. NP-40 soluble and insoluble fractions of claudins were examined by Western blot. Voluntary movement was significantly lower in the oesophagitis model rats than in the sham-operated rats (P < 0.01). Although omeprazole reduced the size of erosions, it did not significantly affect the total amount of voluntary movement (r = -0.033, P = 0.916). Intracellular spaces were significantly dilated in the oesophagitis model rats and claudin-3 showed a significantly lower relative quantity in the NP-40 insoluble fraction. Omeprazole significantly increased voluntary movement of oesophagitis model rats and the relative quantity of claudin-3 in the insoluble fraction (P < 0.05). Dilated intercellular spaces and the lower level of claudin-3 may relate to the voluntary movement of oesophagitis model rats. Decreases in voluntary movement of oesophagitis model rats may reflect visceral symptoms and be able to serve as an index of chronic abdominal symptoms.
authors.affiliation: Division of Upper Gastroenteroelogy, Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan. miwahgi@hyo-med.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Miwa
authors.forename: T
authors.initials: T
authors.lastname: Oshima
authors.forename: J
authors.initials: J
authors.lastname: Sakurai
authors.forename: T
authors.initials: T
authors.lastname: Tomita
authors.forename: T
authors.initials: T
authors.lastname: Matsumoto
authors.forename: S
authors.initials: S
authors.lastname: Iizuka
authors.forename: J
authors.initials: J
authors.lastname: Koseki
mesh_terms: D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology / Q000627:therapeutic use; D062465:Claudin-3; D062506:Claudin-4; D004195:Disease Models, Animal; D004942:Esophagitis, Peptic / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D004947:Esophagus / Q000033:anatomy & histology / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D009853:Omeprazole / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000897:Anti-Ulcer Agents; D062465:Claudin-3; D062506:Claudin-4; C568124:Cldn3 protein, rat; D008565:Membrane Proteins; D009853:Omeprazole