HYPOXIA-INDUCED NECROTIZING ENTEROCOLITIS IN THE IMMATURE RAT - THE ROLE OF LIPID-PEROXIDATION AND MANAGEMENT BY VITAMIN-E

The authors developed an experimental model of necrotizing enterocolit is (NEC) by hypoxia reoxygenation, and determined the content of malon dialdehyde levels as an index of lipid peroxidation, related with a fr ee-radical reaction in the gastrointestinal tract of newborn rats. The y also investigated the role of vitamin E, an antioxidant, in this fre e-radical injury. The study was performed on 1-day-old rats. The 30 ra t 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 sub jected to hypoxia-reoxygenation and killed 3 days after hypoxia. Group 2 (n = 10) was subjected to hypoxia reoxygenation and treated with vi tamin 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 i njury and ranged from superficial epithelial damage with villous short ening to transmural necrosis. In the vitamin E-treated animals these l esions were milder. The malondialdehyde levels of group 1 were signifi cantly higher than those of the other two groups (P < .001). This stud y shows that oxidant-mediated lipid peroxidation injury plays a centra l role in mediating hypoxia-induced intestinal necrosis and suggests t hat vitamin E may play a therapeutic role in NEC. Copyright (C) 1995 b y W.B. Saunders Company.