title: Delayed gastric emptying and disruption of the interstitial cells of Cajal network after gastric ischaemia and reperfusion.
abstract: BACKGROUND
  Gastrointestinal tract is one of the most susceptible organ systems to ischaemia. Not only mucosal injury but also alterations of the intestinal motility and loss of interstitial cells of Cajal (ICC) have been reported in response to ischaemia and reperfusion (I/R). However, there are few reports on the changes in the gastric motility after gastric I/R. The present study was designed to investigate the alterations in gastric emptying, the ICC and enteric nerves that regulate smooth muscle function in response to gastric I/R.
  
  
  METHODS
  Seven-week-old male Wistar rats were exposed to gastric I/R, and the gastric emptying rates at 12 and 48 h after I/R were evaluated by the phenol red method. Expressions of gene product of c-kit receptor tyrosine kinase (c-Kit), a marker of ICC, and of neuronal proteins were also examined.
  
  
  RESULTS
  Gastric emptying was transiently delayed at 12 h after I/R, but returned to normal by 48 h. Expression of c-Kit protein as assessed by Western blotting and immunofluorescent staining of the smooth muscle layer, as well as expression of the mRNA of stem cell factor, the ligand for c-Kit, were reduced at both 12 and 48 h after I/R. The expression of neuronal nitric oxide synthase (nNOS) protein as assessed by Western blotting and immunofluorescent staining was also decreased at 12 h after I/R, but was restored to normal by 48 h.
  
  
  CONCLUSIONS
  Gastric I/R evokes transient gastroparesis with delayed gastric emptying, associated with disruption of the ICC network and nNOS-positive neurons.
authors.affiliation: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Horiguchi
authors.forename: H
authors.initials: H
authors.lastname: Tsugawa
authors.forename: J
authors.initials: J
authors.lastname: Matsuzaki
authors.forename: T
authors.initials: T
authors.lastname: Takagi
authors.forename: N
authors.initials: N
authors.lastname: Shimojima
authors.forename: T
authors.initials: T
authors.lastname: Hibi
mesh_terms: D000818:Animals; D015153:Blotting, Western; D005455:Fluorescent Antibody Technique; D005746:Gastric Emptying; D005753:Gastric Mucosa / Q000378:metabolism; D056885:Interstitial Cells of Cajal / Q000378:metabolism*; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008854:Microscopy, Electron; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013270:Stomach / Q000098:blood supply* / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D052248:Nitric Oxide Synthase Type I; D019009:Proto-Oncogene Proteins c-kit