Renal apoptosis following carbon dioxide pneumoperitoneum in a rat model

Laparoscopically recruited kidneys regain normal function more slowly than laparotomy harvested organs for several possible reasons. We investigated the effects of CO(2) induced pneumoperitoneum on kidney function, as reflected by blood and urine creatinine levels, and its relation with renal cell apoptosis.

CO(2) pneumoperitoneum was established in anesthetized Wistar male rats that were randomly allocated at 6 per group into 1 of 6 groups with an intraperitoneal pressure of 0 (control), 5, 8, 12, 15 or 18 mm Hg. Pressure was maintained for 60 minutes in all groups. Three additional groups were subjected to 30-minute pneumoperitoneum at 0, 12 and 18 mm Hg, respectively. The rats were kept alive for the ensuing 24 hours, after which blood and urine creatinine were analyzed and the abdominal organs were harvested. Various areas of the organs were analyzed for apoptotic cells using the TUNEL method. Cells were randomly counted in 10 eyeshots in 3 sections each using an ocular micrometer.

Creatinine levels in blood and urine changed as pressure and pneumoperitoneum duration progressed. Isolated TUNEL positive nuclei were detected in the outer medulla and the cortex of control kidneys. There was a significantly higher number of TUNEL positive nuclei in the cortex and the medulla of all pressurized kidneys (p <0.05), which increased in parallel with increasing intraperitoneal pressure and pneumoperitoneum exposure time.

The CO(2) pneumoperitoneum gradient and its duration affect renal function and induce apoptosis. This could be a mechanism involved in renal delayed graft dysfunction in recipients of laparoscopically harvested kidneys.