Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia

被引:17
作者
Brooks, KJ [1 ]
Hargreaves, I
Bhakoo, K
Sellwood, M
O'Brien, F
Noone, M
Sakata, Y
Cady, E
Wylezinska, M
Thornton, J
Ordidge, R
Nguyen, Q
Clemence, M
Wyatt, J
Bates, TE
机构
[1] UCL, Sch Med, Dept Paediat, London WC1E 6JJ, England
[2] Natl Hosp Neurol & Neurosurg, Dept Clin Biochem, London WC1N 3BG, England
[3] Univ London Imperial Coll Sci Technol & Med, Robert Steiner MR Unit, MRC, Ctr Clin Sci,Fac Med, London W12 0NN, England
[4] Univ Coll Hosp NHS Trust, Dept Med Phys & Bioengn, London WC1E 6JA, England
基金
英国医学研究理事会;
关键词
neonatal brain; hypoxia-ischemia; hypothermia; neuroprotection;
D O I
10.1023/A:1021622724485
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effects of normothermia and delayed hypothermia on the levels of N-acetylaspartate (NAA), reduced glutathione (GSH) and the activities of mitochondrial complex I, II-III, IV and citrate synthase were measured in brain homogenates obtained from anaesthetized neonatal pigs following transient in vivo hypoxia-ischaemia. In the normothermic animals there was a significant decrease in complex I activity and in the levels of GSH and NAA when compared to the controls. Delayed hypothermia preserved NAA and GSH at control levels and enhanced the rate of complex II-III activity. There was correlation ( R = 0.79) between GSH and NAA levels when data from all three experimental groups were analyzed. Citrate synthase activity was not significantly different in the three groups, indicating maintenance of mitochondrial integrity. These data suggest that delayed hypothermia affords protection of integrated mitochondrial function in the neonatal brain following transient hypoxia-ischaemia.
引用
收藏
页码:1599 / 1604
页数:6
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