title: Gut luminal microdialysis of glycerol as a marker of intestinal ischemic injury and recovery.
abstract: OBJECTIVE
  To evaluate microdialysis as a method to assess different degrees of intestinal damage and recovery during ischemia and reperfusion; to evaluate information obtained from microdialysis catheters in the peritoneum, the gut wall, and the gut lumen.
  
  
  METHODS
  Randomized, controlled animal experiment.
  
  
  METHODS
  University laboratory animal center.
  
  
  METHODS
  Twenty-seven domestic pigs.
  
  
  METHODS
  The superior mesenteric artery was cross-clamped for 60 mins (n = 14) or 120 mins (n = 10) followed by 2 or 4 hrs of reperfusion. Three pigs served as controls.
  
  
  RESULTS
  Intestinal mucosal integrity was assessed by morphometry, adenosine triphosphate in the gut wall, and permeability of C-polyethylene glycol. Lactate, glycerol, pyruvate, and glucose were measured by microdialysis. Changes in adenosine triphosphate, permeability, or lactate did not correlate to different extents of intestinal damage caused by 60 or 120 mins of ischemia. During the reperfusion period, pigs with 60 mins of intestinal ischemia showed a faster recovery of these variables than pigs with 120 mins of intestinal ischemia. Glycerol increased with increasing duration of the ischemic insult. After 60 mins of intestinal ischemia, glycerol in the gut lumen decreased toward baseline but remained high after 120 mins of intestinal ischemia. There was a good correlation between gut luminal glycerol and recovery of mucosal damage throughout the reperfusion period. In the peritoneal cavity, both glycerol and lactate decreased to baseline relatively shortly after onset of reperfusion independent of the duration of intestinal ischemia.
  
  
  CONCLUSIONS
  Microdialysis of glycerol provides information about the extent and severity of intestinal damage after ischemia and about the ensuing recovery. The gut lumen is to be preferred as a site for placement of microdialysis catheters.
authors.affiliation: Department of Anesthesiology and Intensive Care, St. Olav University Hospital, Norwegian University of Science and Technology, N-7006 Trondheim, Norway. erik.sollegard@ntnu.no
authors.forename: Erik
authors.initials: E
authors.lastname: Solligård
authors.forename: Ingebjørg S
authors.initials: IS
authors.lastname: Juel
authors.forename: Karin
authors.initials: K
authors.lastname: Bakkelund
authors.forename: Per
authors.initials: P
authors.lastname: Jynge
authors.forename: Kåre E
authors.initials: KE
authors.lastname: Tvedt
authors.forename: Harald
authors.initials: H
authors.lastname: Johnsen
authors.forename: Petter
authors.initials: P
authors.lastname: Aadahl
authors.forename: Jon Erik
authors.initials: JE
authors.lastname: Grønbech
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000098:blood supply*; D019344:Lactic Acid / Q000378:metabolism; D017551:Microdialysis; D010537:Peritoneum / Q000378:metabolism; D020127:Recovery of Function / Q000502:physiology; D015427:Reperfusion Injury / Q000378:metabolism*; D013552:Swine
chemical_list: D015415:Biomarkers; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D005990:Glycerol