title: Renal oxidative stress following CO2 pneumoperitoneum-like conditions.
abstract: BACKGROUND
  Physiologic renal changes associated with pneumoperitoneum (PNP) have been described and various underlying mechanisms have been suggested. We investigated the possibility that PNP-associated renal damage is pressure dependent, and that oxidative stress is thereby involved.
  
  
  METHODS
  Seventy Wistar rat kidneys (n=10 per group) were isolated. They were perfused with oxygenated, warm, Krebs-Henseleit solution containing 5% albumin within an isolated environment and subjected to various CO(2) pressures (0 [control], 3, 5, 8, 12, 15, and 18 mmHg) for 60 min. Half of each group was additionally perfused for 30 min at 0 mmHg pressure.
  
  
  RESULTS
  Renal flow decreased proportionately to the applied pressure as did urine output: both decreased (P < 0.05) after 60 and 90 min when pressure >or=8 mmHg was applied. Oxygen extraction decreased (P<0.05) during PNP in all pressurized groups. Xanthine oxidase (XO) activity and reduced glutathione in the tissues increased (P<0.05) proportionately to pressures >or=8 mmHg. All parameters slightly reversed toward baseline values, upon the release of the intra-chamber pressure, except for the 18 mmHg group's values.
  
  
  CONCLUSIONS
  CO(2)-PNP pressure induces kidney injury, possibly reversible immediately after pressure is annulled. Pressure is associated with oxidative stress, which interferes with cellular metabolism and function, possibly via an ischemic-reperfusion-like mechanism.
authors.affiliation: Division of General Surgery B, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel. we_khoury@yahoo.com
authors.forename: Wisam
authors.initials: W
authors.lastname: Khoury
authors.forename: Letizia
authors.initials: L
authors.lastname: Schreiber
authors.forename: Amir
authors.initials: A
authors.lastname: Szold
authors.forename: Joseph M
authors.initials: JM
authors.lastname: Klausner
authors.forename: Avi A
authors.initials: AA
authors.lastname: Wienbroum
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000009:adverse effects*; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism*; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects* / Q000379:methods; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects*; D014563:Urodynamics; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D002245:Carbon Dioxide; D014969:Xanthine Oxidase; D005978:Glutathione; D010100:Oxygen