Dóra E, Zeuthen T, Silver I A, Chance B, Kovách A G
Acta Physiol Acad Sci Hung. 1979;54(4):319-31.
The effect of different degrees of arterial hypoxia on cerebrocortical NAD/NADH redox state, reflectance, oxygen tension, extracellular potassium ion concentration, ECoG and arterial blood pressure was investigated in rats. The results may be summarized as follows. a) The decrease of cortical pO2 preceded the dilatation of cortical vessels by 15-20 sec but the changes in cortical extracellular potassium ion concentration, ECoG and arterial blood pressure started later than the vasodilatation. These results give further support to the regulatory role of cortical pO2 decrease in the initiation of cerebrocortical vasodilatation during arterial hypoxia. b) Since the K+ concentration of the brain cortex and the ECoG did not change in mild arterial hypoxia, the significant NAD reduction obtained in this experimental group is likely to be of cytoplasmic origin. The same conclusion applies to the initial periods of severe arterial hypoxia. On the basis of the extent of NAD reduction during various degrees of arterial hypoxia it is concluded that about 30% of the NAD reduction occurring in anoxia is of cytoplasmic origin. c) When the animals were ventilated with a gas mixture containing 4-7% oxygen, the brain cortex became nearly anoxic, partly because of the gradual decrease of arterial blood pressure. Finally, the mechanism of potassium leakage is identical under prolonged severe arterial hypoxaemia and on anoxic terminal depolarization.
在大鼠中研究了不同程度的动脉低氧对大脑皮质NAD/NADH氧化还原状态、反射率、氧张力、细胞外钾离子浓度、脑电图（ECoG）和动脉血压的影响。结果可总结如下。a）皮质pO2的降低比皮质血管扩张提前15 - 20秒，但皮质细胞外钾离子浓度、ECoG和动脉血压的变化比血管扩张开始得晚。这些结果进一步支持了在动脉低氧期间皮质pO2降低在大脑皮质血管扩张起始中的调节作用。b）由于在轻度动脉低氧时大脑皮质的K+浓度和ECoG没有变化，该实验组中显著的NAD还原可能源于细胞质。这一结论同样适用于重度动脉低氧的初始阶段。根据不同程度动脉低氧期间NAD还原的程度，得出在缺氧时发生的NAD还原约30%源于细胞质。c）当用含4 - 7%氧气的混合气体对动物进行通气时，大脑皮质几乎缺氧，部分原因是动脉血压逐渐降低。最后，在长期重度动脉低氧血症和缺氧终末去极化情况下，钾泄漏的机制是相同的。
