Renal oxidative stress following CO 2 pneumoperitoneum-like conditions Wisam Khoury Æ Letizia Schreiber Æ Amir Szold Æ Joseph M. Klausner Æ Avi A. Wienbroum Received: 25 January 2008 / Accepted: 15 June 2008 Ó Springer Science+Business Media, LLC 2008 Abstract Background Physiologic renal changes associated with pneumoperitoneum (PNP) have been described and various underlying mechanisms have been suggested. We investi- gated the possibility that PNP-associated renal damage is pressure dependent, and that oxidative stress is thereby involved. Materials and 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 C8 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 C8 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 inter- feres with cellular metabolism and function, possibly via an ischemic-reperfusion-like mechanism. Keywords Urology Á Transplantation Changes in renal physiology related to pneumoperitoneum (PNP) have been studied extensively [1, 2]. During PNP, there are transient elevations in creatinine values and decrease in urine output [3–5], and oliguria is more prominent during high pressures and prolonged PNP [4–6]. It was suggested that this is due to transient renal injury associated with reduced renal blood flow and cortical hypoperfusion—all due to the elevated intra-abdominal pressure [7]. The neuroendocrine response to PNP, the high excretion of antidiuretic hormone (ADH) [8, 9], frequent respiratory acidosis, which induces sympathetic stimuli, as well as increased renal vasoconstriction [10], are all con- tributing events. Nevertheless, tubular injury has never been documented under these conditions [11, 12]. The effects of PNP on the kidney may be critical in patients suffering from impaired kidney function or in This paper was presented in part in the 15th EAES, July 2007, Athens, Greece. W. Khoury Á A. Szold Á J. M. Klausner Division of General Surgery B, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel e-mail: we_khoury@yahoo.com A. Szold e-mail: L. Schreiber Department of Pathology and Animal Research Laboratory, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel A. A. Wienbroum (&) Post-Anesthesia Care Unit and Animal Research Laboratory, Tel Aviv Sourasky Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel e-mail: draviw@tasmc.health.gov.il 123 Surg Endosc DOI 10.1007/s00464-008-0054-2