title: Effect of increased abdominal pressure on cytokines (IL1 beta, IL6, TNFalpha), C-reactive protein (CRP), free radicals (NO, MDA), and histology.
abstract: BACKGROUND
  It is generally accepted that proinflammatory mediators, including cytokines, are responsible for the metabolic changes associated with injury. Recent clinical and experimental studies have also shown that the laparoscopic procedures actually produce ischemia-reperfusion injury in the organs by oxygen-derived free radicals. This study aimed to assess the effect of different insufflation pressures and laparotomy on tissue response by comparing the proinflammatory cytokines, C-reactive protein, and serum and tissue levels of oxygen-derived free radicals.
  
  
  METHODS
  Forty mature New Zealand white rabbits were assigned to 4 groups of 10 animals. In groups 1 to 3, CO2 pneumoperitoneum was created using an automatic insufflator to the designated pressure of 10, 15, and 20 mm Hg, respectively. The remaining 10 animals underwent laparotomy using 10 cm midline incision (group 4). Blood samples were collected before (0 min) and at the end of the procedure (60 min). After the collection of last blood samples, all animals were killed and samples from liver and gut were obtained for measurements of tissue malondialdehyde levels and histology.
  
  
  RESULTS
  The proinflammatory cytokine levels were increased significantly in groups 1 to 3, but did not change in the laparotomy group. Serum C-reactive protein levels were elevated in all groups. The comparison of the results between the laparotomy and laparoscopy groups showed that serum interleukin 6 and nitric oxide levels were significantly elevated in relation the intra-abdominal pressure, and serum interleukin 6 and nitric oxide levels peaked in group 3. Tissue malondialdehyde levels were significantly higher in groups 1 and 2 than in groups 3 and 4.
  
  
  CONCLUSIONS
  The findings of our experiment suggest that the elevated intra-abdominal pressure is responsible for ischemia, free radical production, and proinflammatory cytokine response-mediated cell damage during laparoscopic surgery.
authors.affiliation: Department of Surgery, Ankara Numune Teaching and Research Hospital, Ankara, Turkey. mmahir@mynet.com
authors.forename: Mahir M
authors.initials: MM
authors.lastname: Ozmen
authors.forename: Baris
authors.initials: B
authors.lastname: Zulfikaroglu
authors.forename: Cavit
authors.initials: C
authors.lastname: Col
authors.forename: Ismail
authors.initials: I
authors.lastname: Cinel
authors.forename: Ferruh K
authors.initials: FK
authors.lastname: Isman
authors.forename: Leyla
authors.initials: L
authors.lastname: Cinel
authors.forename: Tanju H
authors.initials: TH
authors.lastname: Besler
mesh_terms: D000818:Animals; D002097:C-Reactive Protein / Q000032:analysis*; D005609:Free Radicals; D007249:Inflammation / Q000097:blood / Q000503:physiopathology; D053583:Interleukin-1beta / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis*; D010535:Laparoscopy; D008315:Malondialdehyde / Q000097:blood*; D015428:Myocardial Reperfusion Injury; D009569:Nitric Oxide / Q000097:blood*; D011312:Pressure; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D005609:Free Radicals; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D008315:Malondialdehyde; D002097:C-Reactive Protein