LaManna J C, Light A I, Peretsman S J, Rosenthal M
Brain Res. 1984 Feb 20;293(2):313-8. doi: 10.1016/0006-8993(84)91238-1.
To relate cerebral oxygen sufficiency and insufficiency with arterial oxygen tension, reduction/oxidation responses of the initial and terminal members of the mitochondrial respiratory chain (NADH and cytochrome c oxidase) were recorded in situ by optical techniques when increased cerebral energy use was provoked by direct electrical stimulation. Small decreases in paO2, produced by forced ventilation of hypoxic gas mixtures, resulted in decreased amplitude of the characteristic negative shift in extracellular potential which accompanies such stimulation and smaller oxidative response of NADH and cytochrome oxidase. When paO2 fell below 40-50 Torr, stimulation produced reductive rather than oxidative shifts of the mitochondrial respiratory chain components. The data suggest that when arterial oxygen tension is slightly decreased, compensating mechanisms allow brain function to continue with minimal changes in cortical metabolites and high energy phosphate compounds. When arterial oxygen falls below 40-50 Torr, however, compensation can no longer prevent tissue hypoxia during times of increased energy demand. Thus, hypoxemia is not necessarily synonymous with oxygen insufficiency, but oxygen sufficiency must be defined with due regard to the degree of energy demand.
为了将脑氧充足与不足与动脉血氧张力联系起来，当通过直接电刺激引发脑能量消耗增加时，采用光学技术原位记录线粒体呼吸链起始和末端成员（NADH和细胞色素c氧化酶）的还原/氧化反应。通过低氧气体混合物的强制通气使动脉血氧分压（paO2）略有下降，导致伴随这种刺激的细胞外电位特征性负向偏移幅度减小，以及NADH和细胞色素氧化酶的氧化反应减弱。当paO2降至40 - 50托以下时，刺激导致线粒体呼吸链成分发生还原而非氧化变化。数据表明，当动脉血氧张力略有下降时，代偿机制可使脑功能在皮质代谢物和高能磷酸化合物变化最小的情况下继续维持。然而，当动脉血氧降至40 - 50托以下时，在能量需求增加时，代偿不再能够防止组织缺氧。因此，低氧血症不一定等同于氧不足，但氧充足必须根据能量需求程度来定义。
