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

Abstract

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 hypoxia^{3, 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%.