论文部分内容阅读
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。
In this paper, Mongolian gerbils were used to replicate the model of acute cerebral ischemia-reperfusion and to observe the ultrastructure evolution of hippocampal CA, pyramidal cells in different reperfusion time. Found that reperfusion injury is different from the traditional ischemic lesions, the morphological changes require at least 6 hours before starting to appear, the authors believe that ischemic lesions and reperfusion injury both intracellular oxygen utilization abnormalities, but because of the different mechanisms, so the lesions There are characteristics. The theory of the increase of the production of superoxide anion radicals (0_2 ~ -) in hyperoxic cells induced by abnormal oxygen can explain the essence of reperfusion.