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.


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.


CONCLUSIONS
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.
Ozmen
M Mahir
MM
Department of Surgery, Ankara Numune Teaching and Research Hospital, Ankara, Turkey. mmahir@mynet.com
Zulfikaroglu
Baris
B
Besler
Tanju H
TH
Col
Cavit
C
Cinel
Leyla
L
Cinel
Ismail
I
D000704:Analysis of Variance; D000818:Animals; D007511:Ischemia / Q000209:etiology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D010535:Laparoscopy; D008099:Liver / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D011028:Pneumoperitoneum, Artificial; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014781:Viscera / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology
D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D008315:Malondialdehyde