CO2-Pneumoperitoneum Induces Renal Apoptosis in a Rat Model

Background: Kidneys harvested by laparoscopic donor nephrectomy regain normal function slightly later than laparotomy-harvested organs. Several factors affect the organs after laparoscopic recruitment, which could explain the relatively prolonged period of recovery. We investigate the role of CO2-induced pneumoperitoneum (PNP) on organ dysfunction as expressed by cell apoptosis.
Methods: CO2-PNP was established in 24 anesthetized Wistar male rats, randomly allocated into one of six groups with intraperitoneal pressure was 0 (control), 5, 8, 12, 15 or 18 mmHg. Pressure was maintained for 60 min. The rats were kept alive for the ensuing 24 hours, after which their abdominal organs were harvested. Various areas of the organs were analyzed for apoptotic cells using the TdT-mediated biotin-dUTP nick-end labeling (TUNEL) method. The cells were randomly counted in 10 eye-shots in three sections, using an ocular micrometer.
Results: Very few TUNEL-positive nuclei were detected in the liver, pancreas or spleen. Isolated TUNEL-positive nuclei were detected within the outer medulla of the control kidneys. Significantly higher numbers of TUNEL-positive nuclei were encountered in all pressurized kidneys (P

Session: Podium Presentation

Program Number: S019

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