EFFECT OF ARTERIAL HYPOXIA ON THE CEREBROCORTICAL REDOX STATE, VASCULAR VOLUME, OXYGEN-TENSION, ELECTRICAL-ACTIVITY AND POTASSIUM-ION CONCENTRATION

  • 1 January 1979
    • journal article
    • research article
    • Vol. 54  (4) , 319-331
Abstract
The effect of different degrees of arterial hypoxia on cerebrocortical NAD/NADH redox state, reflectance, O2 tension, extracellular K ion concentration, ECoG [electrocorticogram] and arterial blood pressure was investigated in rats. The decrease of cortical P[partial pressure]O2 preceded the dilatation of cortical vessels by 15-20 s but the changes in cortical extracellular K ion concentration, ECoG and arterial blood pressure started later than the vasodilatation. The regulatory role of cortical pO2 decrease in the initiation of cerebrocortical vasodilatation during arterial hypoxia is supported. Since the K+ concentration of the brain cortex and the ECoG did not change in mild arterial hypoxia, the significant NAD reduction 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 .apprx. 30% of the NAD reduction occurring in anoxia evidently is of cytoplasmic origin. When the animals were ventilated with a gas mixture containing 4-7% O2, the brain cortex became nearly anoxic, partly because of the gradual decrease of arterial blood pressure. The mechanism of K+ leakage is identical under prolonged severe arterial hypoxemia and on anoxic terminal depolarization.