Oxidative stress in lung tissue induced by CO2 pneumoperitoneum in the rat

Background. Clinical trials have found that the pneumoperitoneum has potent ially hazardous side effects. The biochemical basis of organ injury induced by pneumoperitoneum is, however, not well defined. Since oxidative stress is believed to play an important role in many pathological conditions, we s et out to examine oxidative stress markers in the lung, liver, kidney, and pancreas by using a rat model of laparoscopy with CO2 pneumoperitoneum and comparing it to a group with gasless laparoscopy. Methods: Malondialdehyde (for lipid peroxidation), protein-bound carbonyls (for protein oxidation), reduced and oxidized glutathione, and the neutroph il marker myeloperoxidase were evaluated in tissue homogenates at 2 h, 6 h, and 18 h after laparoscopy. Immunoblotting was used to analyze the modific ation of lung proteins by 4-hydroxynonenal at 6 h. Results: Significant lipid peroxidation was found selectively in lungs at 2 h and 6 h after CO2 pneumoperitoneum. This was accompanied by a loss of gl utathione but only minor protein oxidation. Further, lung proteins were cle arly modified by the aldehydic product of lipid peroxidation 4-hydroxynonen al. Myeloperoxidase in lungs increased continuously up to 18 h in both expe rimental groups, but there were higher levels in the group with pneumoperit oneum. Conclusion: Oxidative stress is likely to contribute to the impairment of p ulmonary function after laparoscopic operations using a CO2 pneumoperitoneu m.