实验性海马急性缺血与再灌流损伤的电镜观察

本文迭用蒙古沙土鼠复制急性脑缺血再灌流模型,并动态观察海马CA,区锥体细胞在不同再灌流时间内超微结构的演变。发现再灌流损伤不同于传统的缺血病变,其形态改变至少需要6小时才开始出现,作者认为脑缺血病变与再灌流损伤同属细胞内氧的利用异常,但由于机制的不同,故病变各有特征。高氧性细胞内用氧异常致使超氧化物阴离子自由基(0_2~-)产生增多的理论能解释再灌流病变的实质。

ULTRASTRUCTURAL OBSERVATION ON THE EXPERIMENTAL DAMAGE OF HIPPOCAMPUS WITH ACUTE CEREBRAL ISCHEMIA AND REPERFUSION

The CA1 subfield hippocampus of 43 Mongolia gerbils divided into three groups (normal, ischemial and reperfusive) was observed by electron microscopy. All the animals were subjected to bilateral carotid occlusion for 7 min and trans-cardiac perfusion fixation was performed 0, 30, 90min and 3, 6, 12 h or 1, 2, and 4 days afterwards except that 4 gerbils of the normal group were subjected to perfusive fixation only. The result showed that pyramidal cells in CA1 subfield presented a series of changes after ischemia and during reperfusion, From 0 min to 3 h following occlusion, there were no serious lesions, only a light loss was produced, such as "reactive change" and "ischemic cells change". 6 h later, pyramidal cells showed an accumulation of ER. 1 to 4 days later ischemia, the lamellar alignment of proliferated cisterus of the ER and "delayed neuronal death" were the most conspicuous findings in these cells.The result again indicated that the damage of CA1 pyramidal cells is slow and may differ from those which are thought to be typical of ischemic neuronal damage.