title: Hepatic microvascular changes in rat abdominal compartment syndrome.
abstract: BACKGROUND
  Abdominal compartment syndrome (ACS) is associated with an increased rate of multiple organ dysfunction and is an independent marker for mortality. Our objective was to develop an animal model to study the mechanisms of tissue and microvascular injury associated with ACS at the microscopic level.
  
  
  METHODS
  ACS was established in rats with CO₂ insufflation at 20 mm Hg for 2 h, with an abdominal cast. Sinusoidal perfusion, inflammatory response, and cell death were quantified in exteriorized livers. Respiratory and renal dysfunction were assessed biochemically and morphologically. Myeloperoxidase levels, a marker of neutrophil activation, were measured in the liver, lung, and small intestine.
  
  
  RESULTS
  Continuously perfused sinusoids were significantly lower in the ACS group (81.4 ± 2.2% versus 99.6% ± 0.50), with an increase in nonperfused and intermittently perfused sinusoids (P < 0.05). Hepatocellular death and the number of activated leukocytes in postsinusoidal venules showed 7- and 18-fold increases, respectively, in the ACS group (P < 0.05). A significant increase in blood urea nitrogen levels in experimental rats was also observed. Myeloperoxidase levels were found to be 8-fold higher in lungs of ACS rats relative to control (P < 0.05), as well as statistically significant increase in the pCO₂ and decrease in pH of ACS rats.
  
  
  CONCLUSIONS
  We have successfully developed a model of ACS with documented evidence of renal and respiratory dysfunction. In addition, we have microscopy-confirmed evidence of early inflammatory changes and perfusion deficits in the liver with a concomitant increase in cell death in the ACS group.
authors.affiliation: Digestive Disease Institute, Cleveland Clinic Florida, Weston, Florida.
authors.forename: Sami A
authors.initials: SA
authors.lastname: Chadi
authors.affiliation: Centre for Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada.
authors.forename: Hussein
authors.initials: H
authors.lastname: Abdo
authors.affiliation: Centre for Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada; Division of Orthopaedic Surgery, The University of Western Ontario, London, Ontario, Canada. Electronic address: relka.bihari@lhsc.on.ca.
authors.forename: Aurelia
authors.initials: A
authors.lastname: Bihari
authors.affiliation: Division of General Surgery, The University of Western Ontario, London, Ontario, Canada.
authors.forename: Neil
authors.initials: N
authors.lastname: Parry
authors.affiliation: Centre for Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada; Division of Orthopaedic Surgery, The University of Western Ontario, London, Ontario, Canada.
authors.forename: Abdel-Rahman
authors.initials: AR
authors.lastname: Lawendy
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001806:Blood Urea Nitrogen; D059325:Intra-Abdominal Hypertension / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008099:Liver / Q000098:blood supply* / Q000201:enzymology / Q000473:pathology; D008168:Lung / Q000201:enzymology / Q000503:physiopathology; D008297:Male; D008833:Microcirculation; D018715:Microscopy, Video; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015415:Biomarkers; D009195:Peroxidase
keywords: Abdominal compartment syndrome; Carbon dioxide pneumoperitoneum; Liver intravital video microscopy; Microvascular dysfunction