title: Aprotinin reduces oxidative stress induced by pneumoperitoneum in rats.
abstract: BACKGROUND
  Ischemia-reperfusion injury induced by pneumoperitoneum is a well-studied entity, which increases oxidative stress during laparoscopic operations. The reported anti-inflammatory action of aprotinin was measured in a pneumoperitoneum model in rats for the first time in this study.
  
  
  METHODS
  A total of 60 male Albino Wistar rats were used in our protocol. Prolonged pneumoperitoneum (4 h) was applied, causing splanchnic ischemia and a period of reperfusion with a duration of 60 or 180 min followed. Several cytokines and markers of oxidative stress were measured in liver, small intestine, and lungs to compare the aprotinin group with the control group. Tissue inflammation was also evaluated and compared between groups using a five-scaled histopathologic score.
  
  
  RESULTS
  In aprotinin group values of biochemical markers (tumor necrosis factor α, interleukin 6, endothelin 1, C reactive protein, pro-oxidant-antioxidant balance, and carbonyl proteins) were lower in all tissues studied. Statistical significance was greater in liver and lungs (P < 0.05). Histopathologic examination revealed significant difference between control and aprotinin groups in all tissues examined. Aprotinin groups showed mild to moderate lesions, while in control groups severe to very severe inflammation was present. Aprotinin subgroup with prolonged reperfusion period (180 min) showed milder lesions in all tissues than the rest of the groups.
  
  
  CONCLUSIONS
  Aprotinin reduced inflammatory response and oxidative stress induced by pneumoperitoneum in liver, small intestine, and lungs.
authors.affiliation: Second Propedeutical Department of Surgery, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece. Electronic address: baltmin@gmail.com.
authors.forename: Minas
authors.initials: M
authors.lastname: Baltatzis
authors.affiliation: Second Propedeutical Department of Surgery, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Theodoros E
authors.initials: TE
authors.lastname: Pavlidis
authors.affiliation: Second Propedeutical Department of Surgery, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Odysseas
authors.initials: O
authors.lastname: Ouroumidis
authors.affiliation: Department of Biochemistry, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Georgios
authors.initials: G
authors.lastname: Koliakos
authors.affiliation: Department of Pathology, Hippocration Hospital, Thessaloniki, Greece.
authors.forename: Christina
authors.initials: C
authors.lastname: Nikolaidou
authors.affiliation: Department of Pathology, Hippocration Hospital, Thessaloniki, Greece.
authors.forename: Ioannis
authors.initials: I
authors.lastname: Venizelos
authors.affiliation: Department of Biochemistry, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Anna
authors.initials: A
authors.lastname: Michopoulou
authors.affiliation: Second Propedeutical Department of Surgery, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Athanasios
authors.initials: A
authors.lastname: Sakantamis
mesh_terms: D000818:Animals; D007611:Aprotinin / Q000187:drug effects / Q000627:therapeutic use*; D008099:Liver / Q000473:pathology; D008297:Male; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects*; D050050:Protein Carbonylation / Q000187:drug effects*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D013152:Splanchnic Circulation
chemical_list: D015842:Serine Proteinase Inhibitors; D007611:Aprotinin
keywords: Aprotinin; Ischemia–reperfusion injury; Oxidative stress; Pneumoperitoneum