Inoue N, Goto S, Korematsu K, Oyama T, Yamada K, Nagahiro S, Ushio Y
Department of Neurosurgery, Kumamoto University Medical School, Japan.
Acta Neurochir (Wien). 1996;138(9):1126-31. doi: 10.1007/BF01412318.
An enzyme-histochemical technique was used to examine the changes in cytochrome oxidase activity during acute focal ischaemia in the rat. In the somatosensory cortex, the enzyme activity began to increase significantly (p < 0.01) 1 hour after middle cerebral artery occlusion (MCAO) and continued to increase up to 3 hours, during which ischaemic cell damage was not detected. In the striatum, the enzyme activity increased significantly (p < 0.01) 1 hour after MCAO in the absence of morphological evidence of ischaemic cell damage; a peak activity was reached at 2 hours, and began to decline 3 hours after MCAO when moderate ischaemic change was detected. In both cortical and subcortical areas, the enzyme activity tended to decrease from 4 hours after MCAO, and was reduced to a level similar to or below that of the non-ischaemic hemisphere 5 hours after MCAO, when severe ischaemic damage was demonstrated. The relation of this transient increase of cytochrome oxidase activity in the early stage of acute ischaemia and the hypermetabolism of neuronal cells during ischaemic insult was discussed.
采用酶组织化学技术检测大鼠急性局灶性缺血过程中细胞色素氧化酶活性的变化。在体感皮层,大脑中动脉闭塞(MCAO)1小时后酶活性开始显著增加(p<0.01),并持续增加至3小时,在此期间未检测到缺血性细胞损伤。在纹状体,MCAO 1小时后酶活性显著增加(p<0.01),此时尚无缺血性细胞损伤的形态学证据;2小时达到活性峰值,MCAO 3小时后当检测到中度缺血性变化时开始下降。在皮层和皮层下区域,MCAO 4小时后酶活性均呈下降趋势,MCAO 5小时后降至与非缺血半球相似或更低水平,此时出现严重缺血性损伤。文中讨论了急性缺血早期细胞色素氧化酶活性的这种短暂增加与缺血性损伤期间神经元细胞代谢亢进的关系。