The purpose of this experimental study was to investigate whether the increased intraabdominal pressure due to gas insufflation creates intestinal ischemia leading to oxygen free radical production and bacterial translocation. A group of 88 rats were studied, 40 of which were subjected to a 15 mmHg pressure pneumoperitoneum for 60 minutes, with the following parameters being studied: mean arterial pressure after carotid catheterization; intestinal microcirculation by means of the laser-Doppler technique; gut metabolic activity (O2 extraction) by blood sampling from portal vein and carotid artery; intestinal, hepatic, splenic, and lung free radical production (malondialdehyde); and bacterial translocation toward the mesenteric lymph nodes, liver, and spleen at 3 and 18 hours after pneumoperitoneum deflation. The mean arterial pressure exhibited no alterations, whereas the jejunal mucosa microcirculation was significantly decreased (p = 0.0001), as was the gut metabolic activity (p = 0.025). Malondialdehyde was increased in gut mucosa (p = 0.0002), liver (p = 0.02), spleen (p = 0.03), and lung (p = 0.017). Bacterial translocation toward the mesenteric lymph nodes (p = 0.002), spleen (p = 0.002), and liver (p = 0.05) was increased in the 3-hour group; in the 18-hour group bacteria were not found in mesenteric lymph nodes but were in liver (p = 0.008) and spleen (p = 0.035). It is concluded that elevated intraabdominal pressure in the rat leads to intestinal ischemia, oxygen free radical production, and bacterial translocation. These results must be reproduced in humans and their clinical significance clarified.