Study on the pathogenesis of cortical delayd neuronal death after transient cerebral ischemia

点击翻译按钮获取中文摘要

Various mechanisms such as impaired protein synthesis and microcirculatory disturbance have been proposed to explain the mechanism of delayd neuronal death. We examined regional differences in the activity of a mitochondrial respiratory enzyme, succinate dehydrogenase, in normal and postischemic gerbils using the quantitative imaging method.Gerbils of either sex were subjected to 5 min.of bilateral common carotid artery occlusion or permanent occlusion of left common carotid artery, and sacrificed at various time intervals after the ischemia. Some gerbils were sacrificed after a sham procedure. Coronal sections of the forebrain at 1.5mm posterior to the bregma were prepared for quantitative imaging of succinic dehydrogenase (SDH) activity. Histological change was evaluated using the same section after immersion fixation in buffered formalin and staining with HE and KB.In the control gerbils, SD activity in the pyramidal cell layr of the CA 1 sector was lower than in any other area of the hippocampus. In gerbils after transient ischemia, SD activity remained lowest in the Pyramidal cell layr of the CA 1 sector during the examination period. Histologically, selective neuronal necrosis was observed in the Pyramidal layr of the CA 1 sector at 2d and thereafter. After permanent occlusion of the common carotid artery, SDH activity decreased initially at the head of caudate and middle layr of cortex. The area of reduced SDH activity gradually enlarged to the whole area supplied by the ipsilateral carotid artery. Ischemic change by histological examination corresponded to the area of reduced SDH activity. These results showed that poor reserves of respiratory enzyme is the primary factor determining its selective vulnerability.