Petito C K, Babiak T
Ann Neurol. 1982 May;11(5):510-8. doi: 10.1002/ana.410110511.
Transient cerebral ischemia in rats was produced by permanent occlusion of the vertebral arteries and 30-minute occlusion of the common carotid arteries. This model produces ischemic necrosis of neurons in the corpus striatum, cerebral cortex, and hippocampus; infarcts, with necrosis of neuropil, astrocytes, and blood vessels, are rare. Changes in striatal astrocytes at 40 minutes and 3 hours of reperfusion were evaluated by electron microscopy, and quantitative estimates of increases in cytoplasmic and mitochondrial area were performed. In areas of corpus striatum with moderate ischemic cell change, the percentage of astrocytic nuclei increased from 10.79% in controls to 17.76% at 40 minutes after ischemia (p less than 0.01) and 19.86% at 3 hours (p less than 0.01). Astrocytic cytoplasm was expanded and contained increased numbers of mitochondria, many of which were pleomorphic and had dilated intracristal spaces and condensed matrix. Rough endoplasmic reticulum was increased. Total mitochondrial area and number of mitochondrial profiles rose significantly in the astrocytic perikarya and foot processes at 3 hours postischemia. The greater number of astrocytes, the increases in mitochondria and rough endoplasmic reticulum and the configurational changes in the mitochondria suggest increased metabolic activity of astrocytes in postischemic, noninfarcted brain.
通过永久性结扎椎动脉并结扎颈总动脉30分钟来诱导大鼠短暂性脑缺血。该模型可导致纹状体、大脑皮质和海马体中的神经元发生缺血性坏死；梗死灶较少见，伴有神经纤维、星形胶质细胞和血管的坏死。通过电子显微镜评估再灌注40分钟和3小时时纹状体星形胶质细胞的变化，并对细胞质和线粒体面积的增加进行定量估计。在有中度缺血性细胞改变的纹状体区域，星形胶质细胞核的百分比从对照组的10.79%在缺血后40分钟增加到17.76%（p<0.01），在3小时时增加到19.86%（p<0.01）。星形胶质细胞的细胞质扩张，线粒体数量增加，其中许多线粒体形态多样，嵴内间隙扩张，基质浓缩。粗面内质网增加。缺血后3小时，星形胶质细胞的胞体和足突中的线粒体总面积和线粒体轮廓数量显著增加。星形胶质细胞数量增多、线粒体和粗面内质网增加以及线粒体的形态变化表明，缺血后未梗死脑区星形胶质细胞的代谢活性增强。
