目的：少突胶质细胞是脑白质的主要细胞成分，了解少突胶质细胞损伤的病理过程有助于研究早产儿脑损伤的发生机制。该实验目的在于了解3日龄未成熟大鼠双侧颈总动脉结扎造成脑白质损伤后少突胶质细胞超微结构的变化。方法：将3日龄未成熟SD新生大鼠随机分为对照组和实验组。对照组仅切开颈部皮肤，而实验组结扎双侧颈总动脉。术后6，12，24 h分别取实验组和对照组存活大鼠8只，将脑组织的超微切片进行透射电镜检查。结果：对照组存活率为100％，实验组存活率为51%。透射扫描电镜发现实验组大鼠术后6 h脑白质少突胶质细胞普遍水肿，细胞器 (线粒体、内质网、高尔基体)水肿明显，数量减少，线粒体数目减少及水肿尤为多见，有的线粒体出现空泡现象，粗面内质网脱颗粒。术后12 h少突胶质细胞水肿更加明显，细胞器进一步减少,可见细胞核染色质分布不均，少数细胞已经出现核固缩。术后24 h实验组少突胶质细胞广泛核固缩、核溶解, 细胞器广泛缺失。结论：3日龄未成熟大鼠双侧颈总动脉结扎后，大鼠脑白质少突胶质细胞损伤。损伤数小时内少突胶质细胞的细胞器受损，随时间延长进行性加重，直至出现少突胶质细胞核固缩。该研究显示了脑缺血性损伤时，脑白质内少突胶质细胞的超微结构病理变化的全过程。［中国当代儿科杂志，2007，9（3）：225-228］

OBJECTIVE: The oligodendrocyte is a key cell component of brain white matter. It is important to understand the pathology of oligodendrocyte injury to better understand the mechanisms leading to white matter injury in the premature brain. This study investigated the ultrastructural changes of oligodendrocytes following ischemic brain injury in 3-day-old premature rats. METHODS: One hundred and eight 3-day-old Sprague-Dawley (SD) premature rats were randomly divided into experimental and control groups. Ischemic brain injury was induced by ligation of bilateral carotid arteries. The control group underwent a sham operation without carotid ligation. At 6, 12 and 24 hrs after operation, 8 rats were randomly selected from surviving rats of both groups. The brain tissues were sampled for transmission electron microscopy. RESULTS: The survival rate of the control and the experimental groups was 100% and 51%, respectively. At 6 hrs of ischemia, swollen oligodendrocytes were observed in all 8 experimental rats. Organelles, including mitochondria, endoplasmic reticulum, and the Golgi apparatus, were swollen and the number of organelles in all 8 rats decreased noticeably compared with control animals. The swollen and decreased mitochondria were the most frequent change. Vacuolated mitochondria were seen in one rat and degranulated rough endoplasmic reticulum was seen in another rat from the experimental group. At 12 hrs of ischemia, oligodendrocyte swelling and decreased number of organelles became more severe in the experimental group. The oligodendrocyte nuclear chromatin was unevenly distributed and karyopycnosis began to appear in experimental animals. At 24 hrs of ischemia, oligodendrocytes generally displayed karyopycnosis and karyolysis, and organelles disappeared in experimental animals. CONCLUSIONS: Progressive oligodendrocyte damage occurred in 3-day-old premature rats subjected to permanent cerebral ischemia. The organelles injury was observed at 6 hrs of ischemia and evolved to oligodendrocyte apoptosis at 24 hrs of ischemia.［Chin J Contemp Pediatr, 2007, 9 (3):225-228］