【摘要】 目的　研究细胞凋亡在新生儿缺氧缺血性脑损伤（ＨＩＢＤ） 中的作用。　方法　结扎新生７ 日龄大鼠左颈总动脉后吸８％ 浓度氧２ 小时制成ＨＩＢＤ 模型，应用透射电镜、苏木素伊红（ＨＥ）染色、原位缺口末端标记（ＴＵＮＥＬ）综合研究新生大鼠ＨＩＢＤ后脑细胞的死亡形式。　结果　缺氧缺血（ＨＩ）后电镜清晰地观察到神经细胞凋亡各期的形态变化；ＨＥ染色发现ＨＩ后０ 小时左侧纹状体有一些神经元呈凋亡早期的改变；ＨＩ后１８ 小时ＴＵＮＥＬ染色在左脑皮质及纹状体见到阳性凋亡细胞；ＨＩ后２～３ 天凋亡达高峰；持续至少３ 周。　结论　三种方法均表明细胞凋亡为ＨＩＢＤ 后神经元的主要死亡形式，也是加重脑损伤的一个因素。更多还原

【Abstract】 Objective To assess the potential contribution of apoptosis to neuronal death after hypoxic ischemic brain damage(HIBD) in the neonate. Methods The HIBD model was produced in the traditional model of neonatal hypoxia ischemia(HI) which subjected 7 old day Wistar rats to unilateral carotid artery ligation followed by an hypoxic(8% oxygen) episode of 2 hours duration.The patterns of neuronal cell death after cerebral HI injuries were examined in neonatal rat using transmission electron microscopy,Hematoxylin and Eosin(H and E) staining,terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling(TUNEL) staining. Results It was observed clearly by transmission electron microscopy that cell dying by apoptosis underwent a series of morphologic changes.The results showed that some neurons in striatum revealed early morphological characteristics of apoptosis by H and E staining at 0h after HI.The distribution of positive apoptotic cells was not detected in cortex,striatum of the ipsilateral hemisphere until 18h after HI by TUNEL staining.Apoptosis peaked at 2 3d after HI,and persisted for 3 weeks. Conclusion Three methods suggested that apoptosis was major form of cell death after cerebral HI in the neonatal rat,and was also a factor that exacerbated infarct size after HI.更多还原