The hemodynamic effects of CO2-induced pressure on the kidney in an isolated perfused rat kidney model.

Abstract

BACKGROUND: Variable mechanisms were suggested to mediate the changes in renal hemodynamics during pneumoperitoneum. To assess whether it can be pressure dependent only, we conduct a study in an isolated, pressurized, and perfused organ model. METHODS: Seventy Wistar rat kidneys were perfused with oxygenated, 3% albumin-contained Krebs-Henseleit solution. Experiments took place within Plexiglass chamber that provided conditions for perfusion of organs, humidity, and maintenance of intracameral CO2 pressures [0 (control), 3, 5, 8, 12, 15, and 18 mm Hg]. All kidneys (10/group) were perfused for 60 minutes. One-half of the groups were perfused for an additional 30 minutes, during which the perfusion pressures were reduced to 0 mm Hg. pH of the perfusate was measured as well. RESULTS: The perfusion pressure increased and the kidney flow decreased slightly, in proportion with the intrachamber pressure. Urine output decreased to a minimum of 40% in >or=8 mm Hg pressure conditions, compared with the control group. The pH values were below normal, during experimental pneumoperitoneum. CONCLUSIONS: Pneumoperitoneal conditions are a direct cause of changes in renal urinary output. The increase in pCO2 pressure and consequently low intraorgan pH may contribute to a mild transient renal damage during pneumoperitoneum.