Three‐dimensional structural changes in cerebral microvessels after transient focal cerebral ischemia in rats: Scanning electron microscopic study of corrosion casts

Pathological changes of cerebral microvessels in transient ischemia were investigated by scanning electron microscopy of vascular corrosion casts. Wistar rats were treated with middle cerebral artery (MCA) occlusion for 30 min, 1 h,  3 h,  4 h,  5 h  or  7 h  and  subsequent  reperfusion  for 2 h. The ultrastructures of the cast were observed and computer‐aided montage micrographs were obtained for visualization of the whole microvasculature in the ischemic brain hemisphere. Avascular areas representing ischemic areas were detected in the frontotemporal cortex and caudate putamen in the groups from 30 min to 5 h occlusion. Extravasation of the resin, which probably corresponded to the leakage of plasma or hemorrhage, was seen as spheroidal, conglomerative, large massive and worm‐like types. The spheroidal type, which probably indicated a small leakage or minor hemorrhage, began to appear in the 30‐min occlusion group. The conglomerative type, which probably indicated a larger leakage or moderate hemorrhage, appeared in the 3‐ to 5‐h occlusion groups. The large massive and worm‐like types, which probably indicated a significant hemorrhage, appeared in the 4‐ and 5‐h occlusion groups. The number of these extravasations increased significantly in the 4‐h occlusion group. Arterioles near the avascular area frequently showed vasospastic appearances, such as corrugations, fusiform indentations of endothelial nuclei, continuous circulatory constrictions and severe narrowing with interrupted branches. Arteriolar vasospasm possibly caused prolonged hypoperfusion even if reperfusion was achieved. The capillaries had a thin stringy appearance in the 4‐ and 5‐h occlusion groups. These changes seemed to relate closely with increased intracranial pressure by brain edema or hemorrhage. The present study suggested that the risk of brain edema or hemorrhagic infarction increased beyond 3 h of MCA occlusion, and vasospasm of the arterioles might participate in stroke pathophysiology.