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 < 0.01) and 19.86% at 3 hours (p < 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.
ASJC Scopus subject areas
- Clinical Neurology