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

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.