Wagner K R, Kleinholz M, Myers R E
Medical Research Service, Veterans Administration Medical Center, Cincinnati, Ohio 45220.
J Cereb Blood Flow Metab. 1990 May;10(3):417-23. doi: 10.1038/jcbfm.1990.72.
We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of onset of mitochondrial dysfunction and neurologic signs was unclear, in the present study we killed postanoxic cats immediately when signs first appeared. Cerebrocortical homogenates and isolated brain mitochondria only from symptomatic cats showed markedly inhibited substrate-, ADP-, and uncoupler-stimulated respiration rates. Cytochrome oxidase activity and cytochrome aa3 concentrations were also markedly reduced in these mitochondria. Since brain mitochondrial function was impaired when neurologic signs first appeared, mitochondrial alterations are an important early organellar change correlated with development of neurologic deterioration following anoxia.
(a) 在缺氧时血糖过高的猫，以及(b) 出现神经学体征的猫，即复氧后舌部或面部肌肉出现束颤或局灶性癫痫发作。然而，由于线粒体功能障碍的起始时间与神经学体征之间的关系尚不清楚，在本研究中，当体征首次出现时，我们立即处死了缺氧后的猫。仅来自有症状猫的大脑皮质匀浆和分离的脑线粒体显示底物、ADP和解偶联剂刺激的呼吸速率显著受抑制。这些线粒体中的细胞色素氧化酶活性和细胞色素aa3浓度也显著降低。由于当神经学体征首次出现时脑线粒体功能就已受损，线粒体改变是与缺氧后神经功能恶化发展相关的重要早期细胞器变化。
