title: Effects of traumatic brain injury on intestinal contractility.
abstract: BACKGROUND
  Patients with traumatic brain injury (TBI) often suffer from gastrointestinal dysfunction including intolerance to enteral feedings. However, it is unclear how TBI affects small intestinal contractile activity. The purpose of this study was to determine if TBI affects intestinal smooth muscle function.
  
  
  METHODS
  Sprague-Dawley rats were subjected to controlled cortical impact injury (TBI). Sham animals underwent a similar surgery but no injury (SHAM). Animals were sacrificed 1, 3, and 7 days after TBI and intestinal smooth muscle tissue was collected for measurement of contractile activity and transit, NF-kB activity, and cytokine levels. Brains were collected after sacrifice to determine volume loss due to injury.
  
  
  RESULTS
  Contractile activity decreased significantly in ileum, but not jejunum, in the TBI group 7 days after injury compared with SHAM. Brain volume loss increased significantly 7 days after injury compared with 3 days and correlated significantly with the contractile activity 1 day after injury. In the intestinal smooth muscle, NF-kB activity increased significantly in the TBI group 3 and 7 days after injury vs SHAM. Wet to dry weight ratio, indicating edema, also increased significantly in the TBI group. Interleukin-1α, -1β, and -17 increased significantly in the TBI group compared with SHAM.
  
  
  CONCLUSIONS
  Traumatic brain injury causes a delayed but significant decrease in intestinal contractile activity in the ileum leading to delayed transit. The decreased intestinal contractile activity is attributed to secondary inflammatory injury as evidenced by increased NF-kB activity, increased edema, and increased inflammatory cytokines in the intestinal smooth muscle.
authors.affiliation: Department of Pediatric Surgery, University of Texas Medical School at Houston, Houston, TX 77030, USA.
authors.forename: A B
authors.initials: AB
authors.lastname: Olsen
authors.forename: R A
authors.initials: RA
authors.lastname: Hetz
authors.forename: H
authors.initials: H
authors.lastname: Xue
authors.forename: K R
authors.initials: KR
authors.lastname: Aroom
authors.forename: D
authors.initials: D
authors.lastname: Bhattarai
authors.forename: E
authors.initials: E
authors.lastname: Johnson
authors.forename: S
authors.initials: S
authors.lastname: Bedi
authors.forename: C S
authors.initials: CS
authors.lastname: Cox
authors.forename: K
authors.initials: K
authors.lastname: Uray
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000150:complications* / Q000473:pathology; D004195:Disease Models, Animal; D005769:Gastrointestinal Motility / Q000502:physiology*; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D007378:Interleukins / Q000096:biosynthesis; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D009130:Muscle, Smooth / Q000503:physiopathology*; D016328:NF-kappa B / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007378:Interleukins; D016328:NF-kappa B
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