Hypoxia in the central nervous system.
The brain, as a very high energy consumer, is completely reliant on molecular oxygen but because oxygen is dangerous due to toxicity [1], there are mechanisms which allow the brain to exist under low oxygen conditions when 'idling' but increase oxygen delivery when activated. This situation means that the brain can respond naturally to mild hypoxia with acute and chronic adaptive mechanisms. These mechanisms involve systemic and central metabolic and vascular processes that are mediated by hypoxia-inducible factor (HIF)-1. HIF-1-mediated cerebral angiogenesis is completed within 3 weeks of exposure onset and is reversible over the same time frame if normoxia is restored. Hypoxic acclimatizing responses may be significantly impaired with aging and metabolic or vascular disease.
LaManna
Joseph C
JC
Department of Anatomy, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106-4930 USA. joseph.lamanna@case.edu
D000375:Aging; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D002490:Central Nervous System / Q000473:pathology*; D006801:Humans; D000860:Hypoxia; D002534:Hypoxia, Brain; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D051379:Mice; D009389:Neovascularization, Pathologic; D010100:Oxygen / Q000378:metabolism; D011312:Pressure; D013045:Species Specificity; D013997:Time Factors
C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D010100:Oxygen