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. 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 >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.