A modified model of the abdominal compartment syndrome.

Background: To develop an animal model in rats and to investigate whether an intra-abdominal pressure (IAP) of 20 mm Hg will lead to a condition comparable with the abdominal compartment syndrome in humans.

Methods: Forty Sprague-Dawley rats were used. In the study group, IAP was increased to 20 mm Hg using a nitrogen gas pneumoperitoneum for 4 hours. We also observed the next reperfusion period for another 4 hours. In the controls, IAP remained unchanged. Hemodynamic readings, peak inspiratory pressure, renal function parameters, and blood gas were obtained. Additionally, histopathologic examinations were performed.

Results: In the presence of intra-abdominal hypertension (IAH), mean arterial pressure was reduced, whereas central venous pressure was increased significantly. Peak inspiratory pressure remained >35 mbar in the 4 hours of IAH and recovered after decompression. Arterial Po(2) decreased substantially while Pco(2) increased soon after IAH. IAH caused a metabolic acidosis, which was further complicated by the respiratory acidosis. Decompression resulted in normocapnia but the metabolic acidosis persisted. Renal blood flow and urine output decreased obviously, whereas little change was found in blood urea nitrogen and creatinine. The histopathologic study revealed parenchymal injury in lung and intestine.

Conclusions: This animal model was simple and easily reproducible. An IAP of 20 mm Hg can lead to a condition comparable with the abdominal compartment syndrome in humans.