NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia.

The redox state of the anterior suprasylvian gyrus of cats was measured during electrical stimulation and under hypercapnia on cast immobilized and artificially respirated. The state of the nicotinamide adenine dinucleotide-reduced nicotinamide adenine dinucleotide (NAD/NADH) redox system was monitored by in vivo fluorometry. Hypercapnia was produced by inhalation of 10, 15, and 30% CO2, respectively. Hypercapnic acidosis led to NADH oxidation. The NADH oxidation under 30% CO2 inhalation was significantly larger (-14.9 +/- 2.9%) than that observed under 10% (-6.5 +/- 1.9%) and 15% CO2 (-7.0 +/- 1.6%) inhalation. Under normocapnic conditions, stimulation induced NAD reduction to NADH (5.5 +/- 0.8%). The magnitude of the NAD reductive response to stimulation was unaffected by 10% CO2 inhalation, but it was decreased by 15 and 30% CO2 inhalation. The increased concentration of NADH upon stimulation is interpreted as resulting from an increased rate of substrate mobilization. The cause of the oxidation of the NADH pool of the cell during hypercapnia is partly due to the direct inhibitory effect of CO2 on the carbohydrate metabolism, but the role of other mechanisms cannot be neglected either.