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为了探讨新生儿缺氧缺血性脑病（HIE）脑损伤时，是否存在细胞死亡的另一种形式—凋亡（apoptosisApo），选用48只健康新生7天的SD大鼠，建立HIE标准化动物模型，将其随机分为对照组和缺氧缺血后1、4、18、24、40、72h、7天组。应用HE染色、电镜、组织切片原位末端标记技术（TUNEL）等手段，观察和比较各组实验侧脑皮质细胞的凋亡形态、特点和密度。结果光镜和电镜下可见细胞皱缩、核碎裂、Apo小体；原位标记显示实验侧皮质、海马回、丘脑均有末端标记阳性的细胞，证实HIE中的Apo现象。8组皮质区阳性细胞数／mm2F＝109．21P＜0．001。两两比较结果：各级之间P＜0．001。说明缺氧缺血可引起脑细胞凋亡，其强度与细胞凋亡有明显统计学意义。其中在皮质区18h点标记细胞最明显，Apo出现早于坏死，在缺氧缺血脑损伤的早期。提示机体在遭遇病理因素时，首先启动自身内部机制，让部分细胞主动性的死亡。
In order to investigate whether there is apoptosis apoptosis in another kind of brain injury of neonatal hypoxic-ischemic encephalopathy (HIE), 48 healthy neonatal SD rats aged 7 days were used to establish HIE normalized animal model , Were randomly divided into control group and hypoxia-ischemia 1,4,18,24,40,72h, 7 days group. HE staining, electron microscopy and TUNEL were used to observe and compare the apoptotic morphology, characteristics and density of cerebral cortex in each group. Results Cell shrinkage, nuclear fragmentation and Apo bodies were observed under light microscope and electron microscope. The in situ markers showed that the experimental side of the cortex, hippocampus and thalamus had positive end-labeled cells, confirming the Apo phenomenon in HIE. 8 groups of cortical area positive cells / mm2F = 109.21P <0.001. Pairwise comparisons: P <0.001 between levels. Hypoxic-ischemic brain damage can cause apoptosis, its intensity and apoptosis were statistically significant. Among them, the labeled cells were the most obvious at 18h of cortex, and Apo appeared earlier than necrosis in the early stage of hypoxic-ischemic brain damage. Prompt the body in the event of pathological factors, the first to start its own internal mechanism, so that part of the initiative of cell death.