Martin L J, Brambrink A, Koehler R C, Traystman R J
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA.
J Comp Neurol. 1997 Jan 13;377(2):262-85. doi: 10.1002/(sici)1096-9861(19970113)377:2<262::aid-cne8>3.0.co;2-1.
Cerebral hypoxia-ischemia causes encephalopathy and neurologic disabilities in newborns by unclear mechanisms. We tested the hypothesis that hypoxia-ischemia causes brain damage in newborns that is system-preferential and related to regional oxidative metabolism. One-week-old piglets were subjected to 30 minutes of hypoxia and then seven minutes of airway occlusion, producing asphyxic cardiac arrest, followed by cardiopulmonary resuscitation and four-day recovery. Brain injury in hypoxic-ischemia piglets (n = 6) compared to controls (n = 5) was analyzed by hematoxylin-eosin, Nissl, and silver staining, relationships between regional vulnerability and oxidative metabolism were evaluated by cytochrome oxidase histochemistry. Profile counting-based estimates showed that 13% and 27% of neurons in layers II/III and layers of somatosensory cortex had ischemic cytopathology, respectively; CA1 neuronal perikarya appeared undamaged, and < 10% of CA3 and CA4 neurons were injured; and neuronal damage was 79% in putamen, 17% in caudate, but nucleus accumbens was undamaged. Injury was found preferentially in primary sensory neocortices (particularly somatosensory cortex), basal ganglia (predominantly putamen, subthalamic nucleus, and substantia nigra reticulata), ventral thalamus, geniculate nuclei, and tectal nuclei. In sham piglets, vulnerable region generally had higher cytochrome oxidase levels than less vulnerable areas. Postischemic alterations in cytochrome oxidase were regional and laminar, with reductions (31-66%) occurring in vulnerable regions and increases (20%) in less vulnerable areas. We conclude that neonatal hypoxia-ischemia causes highly organized, system-preferential and topographic encephalopathy, targeting regions that function in sensorimotor integration and movement control. This distribution of neonatal encephalopathy is dictated possibly by regional function, mitochondrial activity, and connectivity.
脑缺氧缺血通过尚不明确的机制导致新生儿脑病和神经功能障碍。我们检验了这样一个假说:缺氧缺血导致新生儿脑损伤具有系统偏好性,并与局部氧化代谢相关。对一周龄仔猪施加30分钟缺氧,随后进行7分钟气道阻塞,引发窒息性心脏骤停,接着进行心肺复苏并恢复四天。通过苏木精-伊红染色、尼氏染色和银染色分析缺氧缺血仔猪(n = 6)与对照组(n = 5)的脑损伤情况,通过细胞色素氧化酶组织化学评估局部易损性与氧化代谢之间的关系。基于轮廓计数的估计显示,体感皮层II/III层和各层中分别有13%和27%的神经元具有缺血性细胞病理学改变;CA1神经元胞体未受损,CA3和CA4神经元中受损的不到10%;壳核中的神经元损伤为79%,尾状核中为17%,但伏隔核未受损。损伤优先出现在初级感觉新皮层(尤其是体感皮层)、基底神经节(主要是壳核、丘脑底核和黑质网状部)、腹侧丘脑、膝状体核和顶盖核。在假手术仔猪中,易损区域的细胞色素氧化酶水平通常高于不易损区域。缺血后细胞色素氧化酶的改变具有区域和层状特征,易损区域出现降低(31 - 66%),不易损区域出现升高(20%)。我们得出结论,新生儿缺氧缺血会导致高度有组织、系统偏好性和地形性的脑病,其靶向区域在感觉运动整合和运动控制中发挥作用。新生儿脑病的这种分布可能由区域功能、线粒体活性和连接性决定。