GUT ISCHEMIA, OXIDATIVE STRESS, AND BACTERIAL TRANSLOCATION IN ELEVATED ABDOMINAL PRESSURE IN RATS

The purpose of this experimental study was to investigate whether the increased intraabdorninal pressure due to gas insufflation creates int estinal ischemia leading to oxygen free radical production and bacteri al translocation. A group of 88 rats were studied, 40 of which were su bjected to a 15 mmHg pressure pneumoperitoneum for 60 minutes, with th e following parameters being studied: mean arterial pressure after car otid catheterization; intestinal microcirculation by means of the lase r-Doppler technique; gut metabolic activity (O-2 extraction) by blood sampling from portal vein and carotid artery; intestinal, hepatic, spl enic, and lung free radical production (malondialdehyde); and bacteria l translocation toward the mesenteric lymph nodes, liver, and spleen a t 3 and 18 hours after pneumoperitoneum deflation. The mean arterial p ressure exhibited no alterations, whereas the jejunal mucosa microcirc ulation was significantly decreased (p = 0.0001), as was the gut metab olic activity (p = 0.025). Malondialdehyde was increased in gut mucosa (p = 0.0002), liver (p = 0.02), spleen (p = 0.03), and lung (p = 0.01 7). Bacterial translocation toward the mesenteric lymph nodes (p = 0.0 02), spleen (p = 0.002), and liver (p = 0.05) was increased in the 3-h our 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 i s concluded that elevated intraabdominal pressure in the rat leads to intestinal ischemia, oxygen free radical production, and bacterial tra nslocation. These results must be reproduced in humans and their clini cal significance clarified.