Relationship Between Steady Redox State and Brain Activation-Induced NAD/NADH Redox Responses
It is well recognized that activation of the brain leads to an overwhelming increase in cerebral blood flow (CBF), oxygen, and glucose consumption (Siesjö, 1978; Sokoloff, 1981). Because ATP usage is augmented, the ratio of ATP/ADP decreases, and according to the in vitro data of Chance and Williams (1955), the rate of mitochondrial electron transport and ADP phosphorylation will be accelerated. Consequently, mitochondrial NADH should be oxidized (Chance and Williams, 1955). The increased need of mitochondrial electron transport for reducing equivalents is matched by the increased production of pyruvate via stimulation of glycogenolysis and glycolysis (Siesjö, 1978; Sokoloff, 1981). Though it is unlikely that brain suffers from hypoxia under augmented electrical activity (Siesjö, 1978), a considerable amount of pyruvate is converted into lactate, and NADH accumulates in the cytosol (Howse and Duffy, 1975; Siesjö, 1978). This NADH reduction is explained as being due to the restriced capability of the so-called “H-shuttle” mechanisms to transfer H+ from cytosolic NADH to mitochondrial NAD (Howse and Duffy, 1975; Siesjö, 1978). Interestingly, when the mitochondrial NAD/NADH ratio has been determined with the oxidized-reduced substrate ratio method during epileptic seizures, discernible NADH oxidation was not obtained (Siesjö, 1978).
KeywordsCerebral Blood Flow Redox State Mean Arterial Blood Pressure Brain Cortex NADH Oxidation
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