Ischemia/reperfusion injury plays an important role in the pathogenesis of abdominal compartment syndrome, which is characterized by increased intra-abdominal pressure. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the reperfusion injury after decompression of acute abdominal hypertension. This study was carried out in Wistar albino rats. With the rats under anesthesia, an arterial catheter was inserted intraperioneally and with the use of an aneroid manometer connected to the catheter, intra-abdominal pressure was kept at 20 mm Hg (ischemia group) for 1 hour. In the ischemia/reperfusion group, pressure applied for 1 hour was decompressed and a 1-hour reperfusion period was allowed. In another ischemia/reperfusion group, octreotide was administered (50 μg/kg intraperitoneally) immediately before the decompression of intra-abdominal pressure. At the end of the experiment, liver and intestinal tissues were taken and malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels andmyeloperoxidase (an index of tissue neutrophil inflltration) activity were estimated. The results demonstrated that tissue levels of malondialdehyde and myeloperoxidase activity were elevated, whereas glutathione levels were reduced in both the ischemia and ischemia/reperfusion groups. Octreotide treatment reversed these oxidant responses. In conclusion, increased intra-abdominal pressure causes oxidative organ damage and octreotide, by controlling the reperfusion of abdominal organs and inhibiting neutrophil inflltration, could improve the reperfusioninduced oxidative damage. Therefore its therapeutic role as a “reperfusion injury-limiting” agent must be further elucidated in intra-aortic pressure-induced abdominal organ injury.