Cerebral white matter is highly vulnerable to ischemia

Cerebral white matter is highly vulnerable to ischemia
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DOI:
10.1161/01.str.27.9.1641
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发表时间:
1996-09-01
期刊:
影响因子:
8.3
通讯作者:
Gutierrez, JA
Gutierrez, JA
中科院分区:
医学1区
文献类型:
--
作者:
Pantoni, L;Garcia, JH;Gutierrez, JA

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背景和目的缺血对脑白色物质结构的影响很少被研究,可能是因为白色物质通常被认为比灰质更不易于缺血。本研究的目的是评估早期(小于或等于24小时)实验性局灶性缺血对大鼠脑白色物质的结构影响,作为研究以选择性损伤白色物质为特征的未知发病机制的人类状况的初步步骤。大脑中动脉被血管内细丝阻塞了0.5到24小时。大脑皮质下的白色物质样品进行了检查,光镜和电镜方法,并与图像分析system.Results定量异常早在30分钟后动脉闭塞,有明显肿胀的少突胶质细胞和星形胶质细胞,3小时后,大量的少突胶质细胞被致命的损伤。这些变化发生在皮层和基底神经节出现坏死神经元之前数小时。缺血24 h后,脑白色物质明显变淡,反映有髓轴突节段性肿胀,髓鞘与轴膜间间隙形成,星形胶质细胞肿胀。结论脑白色物质对局灶性脑缺血的影响非常敏感。少突胶质细胞和有髓轴突的病理变化出现较早,似乎是伴随着,但独立于,神经元核周损伤。局灶性缺血的实验模型的修改可以提供的手段来测试的假设,选择类型的人类白质脑病有一个缺血性的起源。
Background and Purpose The effects of ischemia on the cerebral white matter structure seldom have been studied, possibly because white matter is generally considered less vulnerable to ischemia than gray matter. The objective of this study was to evaluate the early (less than or equal to 24 hours) structural effects of experimental focal ischemia on the cerebral white matter of the rat as a preliminary step to investigating human conditions of unknown pathogenesis that are characterized by selective damage to the white matter.Methods Twenty-eight rats, including four Controls, had a middle cerebral artery occluded with an intravascular filament for periods ranging between 0.5 and 24 hours. Brain samples from the subcortical white matter were examined with light and electron microscopic methods, and the abnormalities were quantified with an image-analysis system.Results As early as 30 minutes after the arterial occlusion, there was conspicuous swelling of oligodendrocytes and astrocytes; after 3 hours, large numbers of oligodendrocytes were lethally injured. These changes preceded by several hours the appearance of necrotic neurons in the cortex and basal ganglia. Vacuolation and pallor of the white matter were very marked after 24 hours and reflected the segmental swelling of myelinated axons, the formation of spaces between myelin sheaths and axolemma, and astrocyte swelling.Conclusions These results suggest that the cerebral white matter is highly vulnerable to the effects of focal ischemia. Pathological changes in oligodendrocytes and myelinated axons appear early and seem to be concomitant with, but independent of, neuronal perikaryal injury. Modifications of this experimental model of focal ischemia could provide the means to test the hypothesis that selected types of human leukoencephalopathies have an ischemic origin.