• M Sare, D Hamamci, I Yilmaz, M Birincioglu, B B Mentes, M Ozmen, and O Yesilada.
• Department of Surgery, Gazi University, Faculty of Medicine, Besevler, 06510, Ankara, Turkey. msare@med.gazi.edu.tr
• Surg Endosc. 2002 Jan 1; 16 (1): 188-92.

BackgroundThe purpose of this study was to investigate the possible effects of carbon dioxide (CO2) pneumoperitoneum on free radical formation and lipid peroxidation in the lung and liver tissues of rats.MethodsFor this study, 50 male Sprague-Dawley rats were divided into five equal groups: control (group 1); sham operation (group 2); 5, 10, or 15 mmHg (group 3, 4, or 5) pneumoperitoneum with CO2 groups. At the end of the procedures, the rats were killed, and perfusion was performed via vena jugularis with cold Ringer's lactate. After the perfusion procedure, the lung and liver were harvested, and the supernatant fractions of the lungs and livers were assayed for superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA).ResultsBoth the lung and liver CAT activities were elevated consistently and significantly in the order of the study groups, as compared with the previous groups (p < 0.01 for all comparisons). The lung and liver SOD levels were elevated in groups 4 and 5, as compared with the other groups (p < 0.05). The lung MDA was significantly higher in groups 3 and 4, but not in group 5. Significant elevation in liver MDA was noted only in the 5-mmHg pnemoperitoneum group (p < 0.05).ConclusionsThese results indicate that CO2 pneumoperitoneum applied with 5, 10, or 15 mmHg pressure increases the formation of free oxygen radicals, which is counterbalanced by increased SOD and CAT activities of the lung and liver tissues. This effect of CO2 pneumoperitoneum on free radicals and lipid peroxidation appears to be pressure dependent in rats. The mechanism underlying this pressure dependency is still under investigation.

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