The brain has high metabolic demands and depends on a continuous source of oxygenated blood that contains glucose, the exclusive substrate required for central nervous system (CNS) energy metabolism. Oxygen is vital in this process because oxidative phosphorylation is the major contributor of adenosine triphosphate (ATP), the energy source needed to maintain cellular function. Cerebral hypoxia, typically due to respiratory or cardiovascular causes, deprives the brain of the ability to produce a sufficient amount of energy to sustain its high metabolic demands. Continued hypoxia leads to cell injury and death by a variety of neurotoxic cascades that remain to be fully elucidated. Cerebral hypoxia is most commonly due to a combination of both hypoxemia and hypoperfusion. It is unlikely that pure arterial hypoxemia ever causes CNS tissue injury and death because, at very severe levels of hypoxemia, cardiovascular depression and hypotension usually occur. The challenge is to discover if there is a way to intervene in these pathways to prevent the cellular destruction and clinical consequences.
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