title: Open versus closed abdomen treatment on liver function in rats with sepsis and abdominal compartment syndrome.
abstract: BACKGROUND
  Despite recent advances in understanding the mechanisms of sepsis and abdominal compartment syndrome (ACS) and of improvements in their management, the mortality rates from these conditions remain high. Few studies have compared liver injuries in patients undergoing open and closed abdomen treatment. The aim of this study was to compare the effects of open versus conservative abdominal closure approaches upon liver function using a controlled and randomized model of intra-abdominal hypertension and sepsis in a rat model.
  
  
  METHODS
  Healthy Sprague-Dawley rats underwent cecal ligation and puncture to induce sepsis, followed by intraperitoneal injection of air to induce intra-abdominal hypertension. Twenty-four hours later, the rats were randomly divided into two groups, one (n = 36) undergoing abdominal closure and the other (n = 36) undergoing open abdomen. Rats were killed after 1 hour, 6 hours, 1 day, 3 days, 5 days, and 7 days. Liver injury was evaluated by Hepatic Injury Severity Scoring. The levels of expression of Toll-like receptor 4 (TLR4), tumor necrosis factor-α, interleukin-6, signaling transducer and activator of transcription 3 mRNA, and suppressor of cytokine signaling 3 mRNA were assayed by reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  The levels of tumor necrosis factor-α, interleukin-6, and signaling transducer and activator of transcription 3 mRNA were higher, and those of TLR4 and suppressor of cytokine signaling 3 mRNA were lower, in the open than in the closed group (p < 0.05 each). Serum concentrations of aspartate aminotransferase and alanine aminotransferase were also lower in the open group (p < 0.05 each).
  
  
  CONCLUSIONS
  Open abdominal management may improve liver regeneration soon after surgery, as well as reducing inflammatory responses, by reducing TLR4 expression.
authors.affiliation: Department of Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Chen
authors.forename: Jianan
authors.initials: J
authors.lastname: Ren
authors.forename: Weiwei
authors.initials: W
authors.lastname: Zhang
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D004195:Disease Models, Animal; D015850:Interleukin-6 / Q000378:metabolism; D059325:Intra-Abdominal Hypertension / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery*; D008111:Liver Function Tests; D008115:Liver Regeneration; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050796:STAT3 Transcription Factor / Q000378:metabolism; D018805:Sepsis / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery*; D015398:Signal Transduction; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D012333:RNA, Messenger; D050796:STAT3 Transcription Factor; C491410:Socs3 protein, rat; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase