JOURNAL OF PEDIATRIC SURGERY, cilt.30, ss.1416-1419, 1995 (SCI İndekslerine Giren Dergi)
The authors developed an experimental model of necrotizing enterocolitis (NEC) by hypoxia reoxygenation, and determined the content of malondialdehyde levels as an index of lipid peroxidation, related with a free-radical reaction in the gastrointestinal tract of newborn rats. They also investigated the role of vitamin E, an antioxidant, in this free-radical injury. The study was performed on 1-day-old rats. The 30 rat pups were divided into three groups. Hypoxia was induced by placing the pups in a 100% carbon dioxide chamber for 5 minutes. The pups were reoxygenated with 100% oxygen for 5 minutes. Group 1 (n = 10) was subjected to hypoxia-reoxygenation and killed 3 days after hypoxia. Group 2 (n = 10) was subjected to hypoxia reoxygenation and treated with vitamin E (30 IU/kg/d intraperitoneally) for the next 3 days, and killed. Group 3 (n = 10) rats served as controls. The histopathology of the intestinal lesions in group 1 animals was characteristic of ischemic injury and ranged from superficial epithelial damage with villous shortening to transmural necrosis. In the vitamin E-treated animals these lesions were milder. The malondialdehyde levels of group 1 were significantly higher than those of the other two groups (P < .001). This study shows that oxidant-mediated lipid peroxidation injury plays a central role in mediating hypoxia-induced intestinal necrosis and suggests that vitamin E may play a therapeutic role in NEC. Copyright (C) 1995 by W.B. Saunders Company.