Abstract
The normal function of the brain is entirely dependent on an adequate supply of oxygen for the provision of ATP via oxidative energy metabolism. But, the presence of oxygen in excess of metabolic needs can be toxic, with especially drastic consequences for an organ such as the brain in which neurons cannot be regenerated once lost. Thus, there are mechanisms that have evolved, apparently in response to these opposing requirements, which control oxygen delivery to the brain so that it is tightly coupled to tissue oxygen consumption, such that energy demand is satisfied but brain oxygen exposure is minimized. This principle of just sufficient oxygen implies that under normal ambient oxygen pressures and normal physiological conditions, regional brain blood flow is relatively low and brain tissue oxygen tension is also low (Sick et al., 1982). Increases in functional energy demand would have to be accompanied by at least transient increases in local oxygen delivery (LaManna et al., 1987).
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