Late glial swelling after acute cerebral hypoxia-ischemia in the neonatal rat: A combined magnetic resonance and histochemical study
Late glial swelling after acute cerebral hypoxia-ischemia in the neonatal rat: A combined magnetic resonance and histochemical study
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DOI：
10.1203/00006450-199707000-00009
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发表时间：
1997-07-01
影响因子：
3.6
通讯作者：
Martin, E
中科院分区：
文献类型：
--
作者：
Rumpel, H;Nedelcu, J;Martin, E
短暂性脑缺氧缺血（HI）后继发性脑损伤是由一系列细胞事件引起的。本研究采用磁共振成像和组织化学相结合的方法研究了7 d龄大鼠瞬时HI致继发性脑损伤时细胞毒性和血管源性水肿的形成。为了引起损伤，21只大鼠接受右颈总动脉结扎，然后暴露于8% O-2 1.5小时。记录13只7 d大鼠连续3 d的表观扩散系数（ADC）和横向弛豫时间（T-2）加权磁共振成像。在HI结束和恢复21小时之间的不同时间间隔杀死8只动物，使用神经元和星形细胞标记物进行组织化学分析。ADC的变化显示在恢复期细胞毒性水肿的演变中具有双相功能。HI结束时，同侧皮质ADC明显降低。复氧后，ADC短暂恢复正常，8-48小时后出现二次下降，但不太明显。此后，ADC稳步上升。从恢复8 h开始，血管源性水肿比例稳步增加，可见T-2延长。21 h时，大多数胶质细胞对胶质原纤维酸性蛋白表现出免疫反应性，细胞体积增大，神经元凋亡。这些结果表明，迟发性脑损伤伴有晚期胶质细胞肿胀，并伴有细胞损伤引起的间质间隙增大。
Secondary brain damage after transient cerebral hypoxia-ischemia (HI) is caused by a cascade of cellular events. In this study, complementary methods of magnetic resonance imaging and histochemistry were used to investigate the formation of cytotoxic and vasogenic edema during secondary brain damage induced by transient HI in 7-d-old rats. To elicit injury, 21 rats underwent right common carotid artery Ligation followed by 1.5 h of 8% O-2 exposure. Sequential apparent diffusion coefficient (ADC) and transversal relaxation time (T-2) weighted mag netic resonance imaging were recorded for up to 3 d in 13 7-d-old rats. Eight animals were killed at various intervals between the end of HI and 21 h of recovery to perform histochemical assays using neuronal and astrocytic markers. Changes of the ADC revealed a biphasic function for the evolution of cytotoxic edema during the recovery period. At the end of HI, the ADC in the ipsilateral cortex was significantly decreased. Upon reoxygenation, it returned transiently to normal followed by a secondary, although less pronounced, decline after 8-48 h. After this, the ADC rose steadily. From 8 h of recovery, the proportion of vasogenic edema steadily increased as indicated by the T-2 prolongation. At 21 h, the majority of glial cells showed immunoreactivity for glial fibrillary acidic protein and were of larger size, whereas the neurons were apoptotic. These results indicate that the delayed cerebral injury is accompanied by late glial swelling in conjunction with an enlarged interstitial space due to cell damage.