Objective: To determine the mechanism by which oliguria develops during raised intra-abdominal pressure secondary to CO2 insufflation, we created a rat pneumoperitoneum model.
Methods: Male Sprague-Dawley rats (n = 67) were organized into three groups. Each group was subjected to abdominal pressures of 0 (control), 5, or 10 mm Hg, over one, two, and four hours. Fourteen additional rats underwent a two-hour period of 10 mm Hg insufflation pressure followed by desufflation to 0 mm Hg. Urine output (UO) and serum creatinine levels were measured both during insufflation at one, two, and four hours, and two, four, ten, and twenty-two hours following its release. These measurements were compared to control values at each time point. Ultrasonic flow probes placed around both the inferior vena cava (IVC) and abdominal aorta during insufflation characterized the effects of increased abdominal pressure on blood flow. The flow rate was determined at insufflation pressures of 0 (control, 100% flow) to 25 mm Hg.
Results: Rats subjected to 10 mm Hg pressure had significant decreases in UO (oliguria) compared to controls for up to four hours (P < 0.01). There were no significant differences in UO in the control or 5 mm Hg groups over each time interval. While a reduction in UO was observed at two, four, and ten hours postrelease, significance was achieved only at ten hours (P < 0.006). By twenty-two hours postrelease, no differences in UO were observed. Serum creatinine elevations declined two hours postdesufflation. IVC flow was reduced by 92.9 percent at 10 mm Hg, while arterial flow decreased by 46.4 percent. Flow was restored to preinsufflation levels after release of pneumoperitoneum.
Conclusions: Oliguria can be produced in rats undergoing pneumoperitoneum. The renal effects of pneumoperitoneum are most likely related to renal vascular insufficiency from central venous compression.