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

被引:71
作者
OKUR, H
KUCUKAYDIN, M
KOSE, K
KONTAS, O
DOGAN, P
KAZEZ, A
机构
[1] ERCIYES UNIV, FAC MED, DEPT BIOCHEM, KAYSERI 38039, TURKEY
[2] ERCIYES UNIV, FAC MED, DEPT PATHOL, KAYSERI 38039, TURKEY
关键词
NECROTIZING ENTEROCOLITIS; ISCHEMIA-REPERFUSION INJURY; LIPID PEROXIDATION; VITAMIN-E;
D O I
10.1016/0022-3468(95)90395-X
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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.
引用
收藏
页码:1416 / 1419
页数:4
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