Pantoni L, Garcia J H, Gutierrez J A
Department of Pathology (Neuropathology), Henry Ford Hospital, Detroit, MI 48202-2689, USA.
Stroke. 1996 Sep;27(9):1641-6; discussion 1647. doi: 10.1161/01.str.27.9.1641.
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 (< or = 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.
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.
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.
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.
缺血对脑白质结构的影响鲜有研究，可能是因为一般认为白质比灰质对缺血的耐受性更强。本研究的目的是评估实验性局灶性缺血对大鼠脑白质的早期（≤24小时）结构影响，作为研究以白质选择性损伤为特征的、发病机制不明的人类疾病的初步步骤。
28只大鼠（包括4只对照大鼠）通过血管内丝线闭塞大脑中动脉0.5至24小时。采用光镜和电镜方法检查皮质下白质的脑样本，并用图像分析系统对异常情况进行量化。
动脉闭塞后30分钟，少突胶质细胞和星形胶质细胞即出现明显肿胀；3小时后，大量少突胶质细胞发生致命损伤。这些变化比皮质和基底节区坏死神经元的出现早数小时。24小时后，白质的空泡化和苍白非常明显，反映了有髓轴突的节段性肿胀、髓鞘与轴膜之间间隙的形成以及星形胶质细胞肿胀。
这些结果表明脑白质对局灶性缺血的影响高度敏感。少突胶质细胞和有髓轴突的病理变化出现较早，似乎与神经元胞体损伤同时发生，但与之无关。对这种局灶性缺血实验模型的改进可为检验某些类型的人类白质脑病起源于缺血这一假说提供手段。
