The correlation between reactive oxygen species and histopathology of the liver, gut, and kidneys in animals with elevated intra-abdominal pressure.

BACKGROUND: Clinical and experimental studies have shown that the laparoscopic procedure provides a typical model of ischemia-reperfusion injury in the organs by oxygen-derived free radicals. A pneumoperitoneum produces ischemia during insufflation and reperfusion during desufflation. The aim of this study was to assess the causative role of free radical-mediated reactions in tissue damage under different intra-abdominal insufflation pressures. MATERIALS AND METHODS: Thirty five mature New Zealand white rabbits were assigned to three groups of 10 animals. In groups 1, 2, and 3, the designated pressures of 10, 15, and 20 mm Hg, respectively. The remaining 5 animals underwent laparotomy, using a 10-cm midline incision taken as group 4 (control). Blood samples were collected before (0 minutes) and at the end of the procedure (60 minutes). After the collection of the last blood samples, all animals were sacrificed and the samples from the liver, kidney, and gut were obtained for histologic evaluation and also measurements of tissue malondialdehyde (MDA) levels. RESULTS: The nitric oxide levels were not changed in groups 1 and 2, but increased significantly in group 3. Tissue MDA levels were significantly higher in groups 1 and 2 than groups 3 and 4. Histopathologic examination of the kidney revealed some findings of reversible hypoxic cell injury, including acute cellular swelling, vascular congestion, and some early findings of irreversible injury, such as lysis of the cytoplasmic membrane in all groups and focal parancymal bleeding area in only group 3 as a consequence of increased pressure. Liver histology revealed cellular swelling and karyorhexis in hepatocytes in group 1, whereas only congestion and sinusoidal dilatation was observed in groups 2 and 3. CONCLUSION: Our experimental study showed that abdominal insufflation causes ischemia and free radical production, which seems responsible for the cell damage that occured during laparoscopic surgery.

Effect of increased abdominal pressure on cytokines (IL1 beta, IL6, TNFalpha), C-reactive protein (CRP), free radicals (NO, MDA), and histology.

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.