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用结扎沙土鼠双侧颈总动脉5分钟,然后使血流再通的方法制作迟发性神经元损伤动物模型。从能量代谢角度观察了动物脑6个分区13种生化指标在缺血前后7个时相的变化情况。结果表明,海马CA_1区有其独特的变化规律,突出地表现为:在缺血后重灌流早期线粒体呼吸功能恢复的延迟性及重灌流后期能量代谢的第二次受损现象。经进一步研究认为,这些功能变化的分子基础与呼吸链复合物活性的可逆性或不可逆性丧失相关,而与呼吸链中细胞色素含量的改变无关。本研究的结论为:线粒体功能紊乱是迟发性神经元损伤发生机理中的启动环节。
The animal model of delayed neuronal injury was made by ligating the common carotid arteries of both sides of gerbils for 5 minutes and then by recanalizing the blood flow. From the perspective of energy metabolism, we observed the changes of thirteen biochemical indexes in 6 sections of animal brain before and after ischemia. The results show that the hippocampal CA 1 region has its own unique variation, which is prominently manifested as the delayed recovery of mitochondrial respiratory function and the second damage of energy metabolism in the early post-ischemic reperfusion period. Further studies suggest that the molecular basis of these functional changes is related to the reversible or irreversible loss of respiratory chain complex activity, regardless of changes in cytochrome content in the respiratory chain. The conclusion of this study is that mitochondrial dysfunction is the initiating link in the mechanism of delayed neuronal injury.