NAD Pools in the Brain Cortex Effect of Reversible Anoxic-Anoxia and Irreversible Anoxic-Ischemia

  • Eors Dora
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 180)


It is well recognized that the brain cortices of arterially normoxic animals are heterogenously supplied with oxygen, cortical oxygen tension can vary between zero and 90 mm Hg11.It is not known, however, whether the cells located in low pO2 microregions (pO2<5 mm Hg) are bioenergetically hypoxic, e.g. their respiration is restricted by the low availability of oxygen.In this context, the data obtained in isolated mitochondria1 and in the intact brain (Koga and Austin9; Rosenthal et al.17) are not consistent. While the respiration and redox state of isolated mitochondria are maintained at normal level even at 0.5 torr oxygen tension1, the mitochondrial NAD, FAD and cytochrome aa3 in the in vivo brain cortex are already reduced by slight or moderate arterial hypoxia3, 9, 17. Because cytochrome aa3 in the brain cortex became reduced when FiO2 (O2% in the respired gas mixture) was diminished from 95% to 20%, Rosenthal et al.17 suggested that the brain cortices of arterially normoxic animals are slightly hypoxic. However, there could be some other explanations, like increased supply of reducing equivalents, acidosis, etc., for the early reduction of mitochondrial respiratory carriers occuring at the alterations of FiO2 between 95% and 10%.


Brain Cortex Dead Animal Vascular Volume Cranial Window NADH Fluorescence 
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Copyright information

© Plenum Press, New York 1984

Authors and Affiliations

  • Eors Dora
    • 1
  1. 1.Cerebrovascular Research CenterUniversity of PennsylvaniaPhyladelphiaUSA

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