Cerebral blood flow change in arterial hypoxemia is consistent with negligible oxygen tension in brain mitochondria.
The regulation of blood flow during neuronal activation is poorly understood. Current explanations of the mismatch between increased blood flow and oxygen consumption during neuronal excitation hold that blood flow must rise more than oxygen consumption to compensate for a low oxygen reserve in brain mitochondria. Contrary to the result of a previous study by Mintun et al. (2001), the present test of the hypothesis revealed no conflicts among the claims of unidirectional blood-brain transfer of oxygen, negligible oxygen in mitochondria, and measurements of cerebral blood flow and oxygen consumption. With a simple compartmental model of oxygen delivery to brain tissue, the test showed that neuronal excitation elicits identical increases of cerebral blood flow in normoxemia and hypoxemia, in complete agreement with the claim of a negligible reserve of oxygen in brain mitochondria in vivo.
Gjedde
Albert
A
Pathophysiology and Experimental Tomography Center, Aarhus University Hospitals, Center of Functionally Integrative Neuroscience, Aarhus University, Aarhus, 8000 Denmark.
D001783:Blood Flow Velocity / Q000502:physiology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology*; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*