title: Gut decontamination reduces bowel ischemia-induced lung injury in rats.
abstract: OBJECTIVE
  To evaluate the effects of gut decontamination on endotoxin, tumor necrosis factor (TNF) levels, and the associated lung injury in a rat model of bowel ischemia.
  
  
  BACKGROUND
  Gut ischemia induces disruption of the intestinal mucosal barrier, allowing translocation of bacteria and endotoxin into the blood, which may trigger a systemic inflammatory response and lung injury.
  
  
  METHODS
  Thirty anesthetized rats were randomized into three groups: (1) ischemia-reperfusion (I/R) alone (a 60-min superior mesenteric artery occlusion and 4 h of reperfusion, n=10); (2) rats that underwent gut decontamination prior to ischemia (I/R+GD, n=10); and (3) control rats (sham operated, n=10). Serum levels of lipopolysaccharide (LPS) and TNF were measured at the end of the experiment. Lung permeability was measured using bovine serum albumin labeled with 125I, and organ injury was assessed histologically.
  
  
  RESULTS
  One hour of bowel ischemia and 4 h of reperfusion (I/R) led to elevations of blood LPS and TNF levels of 0.33+/-0.005 EU/mL and 173+/-56 pg/mL, which were higher than the sham group (p<0.01). Gut decontamination (I/R+GD) significantly attenuated the LPS and TNF generation, 0.09+/-0.005 and 56.2+/-6 pg/mL (p<0.01). Lung injury as assessed by pulmonary permeability index was also reduced by gut decontamination, 2.1+/-0.42 vs 5.3+/-0.82 in the control group (p<0.03). Surprisingly no difference was detected in the number of pulmonary neutrophils in sequestration between the groups.
  
  
  CONCLUSIONS
  Our data suggest that gut decontamination can reduce the generation of LPS, TNF, and the severity of lung damage that often follows ischemia and reperfusion of the intestine in rats.
authors.affiliation: Department of Intensive Care and Anesthesiology, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Israel.
authors.forename: P
authors.initials: P
authors.lastname: Sorkine
authors.forename: O
authors.initials: O
authors.lastname: Szold
authors.forename: P
authors.initials: P
authors.lastname: Halpern
authors.forename: M
authors.initials: M
authors.lastname: Gutman
authors.forename: M
authors.initials: M
authors.lastname: Greemland
authors.forename: V
authors.initials: V
authors.lastname: Rudick
authors.forename: G
authors.initials: G
authors.lastname: Goldman
mesh_terms: D000818:Animals; D018988:Bacterial Translocation; D015824:Blood-Air Barrier / Q000502:physiology; D002417:Cattle; D004359:Drug Therapy, Combination / Q000627:therapeutic use*; D019446:Endotoxemia / Q000517:prevention & control*; D004917:Erythromycin / Q000627:therapeutic use*; D007422:Intestines / Q000098:blood supply / Q000382:microbiology*; D007457:Iodine Radioisotopes; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D017538:Mesenteric Artery, Superior; D008641:Mesenteric Vascular Occlusion / Q000150:complications*; D009355:Neomycin / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications*; D012128:Respiratory Distress Syndrome / Q000517:prevention & control*; D012710:Serum Albumin, Bovine; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D007457:Iodine Radioisotopes; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D012710:Serum Albumin, Bovine; D004917:Erythromycin; D009355:Neomycin