Halmágyi G, Lantos J, Szirmai I, Török B
Acta Chir Acad Sci Hung. 1977;18(4):375-91.
Electric activity of the cerebral cortex and the mesencephalon and pO2 of the brain surface were analysed in 47 dogs after serial periods of cerebral anoxia induced by clamping of the aorta for less than 3 minutes and subsequent reperfusion. After restoring the circulation, characteristic stages were observed in the normalization of cortical electric activity and pO2. Improvement in cortical oxygen utilization progressed parallel to the return of rapid activity, though normalization of the EEG preceded that of oxygen utilization. The relative duration of the stages determined from the pO2 curve and from the parameters of electric activity allowed conclusions concerning the injury of the brain tissue. It is assumed that [1] after ischaemic anoxia an excess perfusion develops in the brain; [2] during anoxia, autoregulation of the cerebral vascular system ceases simultaneously with the disintegration of the oxidative metabolic processes of the brain; [3] restitution of the cortex is indicated more reliably by its oxygen consumption rate than by the normalization of EEG activity.
在47只犬中，通过夹闭主动脉不到3分钟诱导脑缺氧并随后再灌注，连续观察不同时间段后，分析大脑皮层、中脑的电活动以及脑表面的氧分压（pO2）。恢复循环后，观察到皮层电活动和pO2正常化过程中的特征性阶段。皮层氧利用的改善与快速活动的恢复平行进展，尽管脑电图（EEG）的正常化先于氧利用的正常化。根据pO2曲线和电活动参数确定的各阶段相对持续时间，有助于对脑组织损伤作出结论。据推测：[1]缺血性缺氧后，脑内会出现过度灌注；[2]缺氧期间，脑血管系统的自动调节与脑氧化代谢过程的瓦解同时停止；[3]皮层恢复情况通过其氧消耗率比通过EEG活动正常化更可靠地显示出来。
