Linn F, Paschen W, Ophoff B G, Hossmann K A
Exp Neurol. 1987 May;96(2):321-33. doi: 10.1016/0014-4886(87)90050-1.
Mitochondrial function was examined in cats after 1 h of complete cerebral ischemia and subsequent recirculation periods from 15 min to 56 h. During ischemia the NAD-linked respiratory control ratio and the maximal phosphorylation capacity of "free" and synaptosomal mitochondria decreased to 53% to 76% of control values. During postischemic reperfusion to 6 h, mitochondrial function was restored to 80%, remaining less than control throughout the entire investigated recirculation period with a tendency of secondary deterioration from 12 h of reperfusion onward. ADP: O ratios were unaffected during ischemia, but decreased significantly during early recirculation (15 to 30 min), and were completely restored from 45 min reperfusion onward. Correlation with electrophysiologic recordings revealed that mitochondrial dysfunction was not a limiting factor for neurophysiologic recovery during early recirculation (15 to 90 min). When the recirculation period was extended (greater than 3 h), good neurophysiologic recovery was associated with a return of mitochondrial function to control levels; inversely, poor mitochondrial function was correlated with poor neurophysiologic recovery.
在猫经历1小时完全性脑缺血及随后15分钟至56小时的再灌注期后，对其线粒体功能进行了检测。在缺血期间，“游离”和突触体线粒体的NAD相关呼吸控制率及最大磷酸化能力降至对照值的53%至76%。在缺血后再灌注至6小时期间，线粒体功能恢复至80%，在整个研究的再循环期内一直低于对照水平，且从再灌注12小时起有二次恶化的趋势。ADP:O比值在缺血期间未受影响，但在早期再循环（15至30分钟）期间显著下降，并从再灌注45分钟起完全恢复。与电生理记录的相关性显示，线粒体功能障碍在早期再循环（15至90分钟）期间并非神经生理恢复的限制因素。当再循环期延长（大于3小时）时，良好的神经生理恢复与线粒体功能恢复至对照水平相关；相反，线粒体功能不良与神经生理恢复不佳相关。
