Whole Body Hypothermia and Oxidative Stress in Babies With Hypoxic-Ischemic Brain Injury

被引:63
|
作者
Perrone, Serafina
Szabo, Miklos [2 ]
Bellieni, Carlo Valerio
Longini, Mariangela
Bango, Marta [2 ]
Kelen, Dorottya [2 ]
Treszl, Andras [2 ]
Negro, Simona
Tataranno, Maria Luisa
Buonocore, Giuseppe [1 ]
机构
[1] Univ Siena, Dept Pediat Obstet & Reprod Med, Policlin Le Scotte, I-53100 Siena, Italy
[2] Semmelweis Univ, Dept Pediat 1, Budapest, Hungary
关键词
OXYGEN-FREE RADICALS; PROTEIN-BOUND IRON; MODERATE HYPOTHERMIA; CEREBRAL-PALSY; INFLAMMATION; APOPTOSIS; RESPONSES; BIRTH;
D O I
10.1016/j.pediatrneurol.2010.05.009
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
According to increasing evidence, hypothermia can significantly improve outcomes in term neonates manifesting asphyxic insult and hypoxic-ischemic encephalopathy. Oxidative stress plays a key role in hypoxic-ischemic and inflammatory brain injuries. We investigated the impact of hypothermia on oxidative stress in babies with hypoxic-ischemic encephalopathy. Term infants were randomly selected for treatment with moderate whole body hypothermia or standard care on normothermia, after perinatal asphyxia. Total hydroperoxides as biochemical markers of oxidative stress, and C-reactive protein as a marker of inflammation, were assayed in blood samples drown at 6, 12, 24, 48, and 72 postnatal hours. In both hypothermic and normothermic groups, total hydroperoxides and C-reactive protein exhibited a continuous increase in the first days after birth. Nevertheless, a tendency was evident for slower and smaller elevations of total hydroperoxides and C-reactive protein in hypothermic compared with normothermic infants. A significant correlation was observed between total hydroperoxides and C-reactive protein in all patients, indicating an association between inflammation and oxidative stress during asphyxia. The slower increase and lower peaks of total hydroperoxides in the hypothermic group support the hypothesis that postasphyxic oxidative stress may be reduced by hypothermia. (C) 2010 by Elsevier Inc. All rights reserved.
引用
收藏
页码:236 / 240
页数:5
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