title: Intestinal injury after thoracic aortic cross-clamping in the pig.
abstract: BACKGROUND
  The mucosal surface epithelium is an essential part of the functional intestinal barrier, but its structural response to ischemia/reperfusion is only partly characterized. The purpose of this study was to provide a detailed morphological evaluation of intestinal surface epithelium after aortic cross-clamping.
  
  
  METHODS
  Pigs were subjected to thoracic aortic cross-clamping for 60 min and subsequent reperfusion for 120 min. Tissue blood flow and high-energy phosphates were measured with microspheres and HPLC, respectively. Urinary excretion of (14)C polyethylene glycol (MW 4000 Da) (PEG-4000), loaded into an intestinal loop, provided an index of intestinal permeability.
  
  
  RESULTS
  Jejunal blood flow was restored at 10 min after aortic declamping. Denudation of the basement membrane of the intestinal villi tips, as a consequence of epithelial shedding, increased markedly during the initial 60 min of reperfusion (P = 0.002). During the following 45 min, the denuded basement membrane was partly covered with low cuboidal and squamous-shaped cells extending lamellipodia over a wavy basement membrane. Restoration of ATP at 60 min after aortic declamping correlated inversely to the extent of denuded basement membrane (r = 0.75, P = 0.032). Permeability of PEG-4000 increased markedly after aortic declamping and was linearly correlated to the area of denuded basement membrane (r = 0.87, P = 0.01).
  
  
  CONCLUSIONS
  Reperfusion for 2 h after aortic cross-clamping is associated with initial aggravation of ischemia-induced injury in the porcine jejunum, but thereafter with restitution of the surface epithelium. Restoration of ATP may be important to avoid intestinal injury after ischemia. Increased permeability of a macromolecule in response to reperfusion is closely correlated to injury of the surface epithelium.
authors.affiliation: Department of Surgery, St. Olav University Hospital, N-7006 Trondheim, Norway. ingebjorg.juel@medisin.ntnu.no
authors.forename: Ingebjørg S
authors.initials: IS
authors.lastname: Juel
authors.forename: Erik
authors.initials: E
authors.lastname: Solligård
authors.forename: Oddveig
authors.initials: O
authors.lastname: Lyng
authors.forename: Tonje
authors.initials: T
authors.lastname: Strømholm
authors.forename: Kåre E
authors.initials: KE
authors.lastname: Tvedt
authors.forename: Harald
authors.initials: H
authors.lastname: Johnsen
authors.forename: Per
authors.initials: P
authors.lastname: Jynge
authors.forename: Ola D
authors.initials: OD
authors.lastname: Saether
authors.forename: Petter
authors.initials: P
authors.lastname: Aadahl
authors.forename: Jon Erik
authors.initials: JE
authors.lastname: Grønbech
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic; D006439:Hemodynamics; D007413:Intestinal Mucosa / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D007583:Jejunum / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D010539:Permeability; D011168:Portal System / Q000503:physiopathology; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D013525:Surgical Instruments / Q000009:adverse effects*; D013552:Swine
chemical_list: D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate