Cerebral energy metabolism in mallard ducks during apneic asphyxia: the role of oxygen conservation.
Cerebral energy metabolism during apneic asphyxia was studied in ducks. Fluctuations in the reduced form of respiratory chain nicotinamide adenine dinucleotide (NADH) were monitored from the left cerebral hemisphere and used as an indicator of mitochondrial hypoxia. Electroencephalogram (EEG) and surface PO2 were recorded from the right hemisphere. Forced dives of 4- to 7-min duration on restrained ducks were characterized by bradycardia and an accumulation of NADH, which increased throughout the diving period. NADH returned to the preasphyxic level when breathing was resumed. In later experiments, asphyxia was produced by stopping artificial ventilation in paralyzed ducks. Asphyxia produced by this means caused similar changes in the measured variables (heart rate, blood pressure, and NADH fluorescence) to those obtained in forced submergence of nonparalyzed ducks. The inhibition of cardiovascular adjustments by atropine caused NADH to increase faster and tissue PO2 to decrease faster during apneic asphyxia than in nonatropinized ducks. We conclude that the oxygen-conserving cardiovascular adjustments play a key role in the increased cerebral tolerance to apneic asphyxia in ducks.
D000818:Animals; D001049:Apnea / Q000378:metabolism*; D001237:Asphyxia / Q000378:metabolism*; D001285:Atropine / Q000494:pharmacology; D002320:Cardiovascular Physiological Phenomena; D002540:Cerebral Cortex / Q000378:metabolism*; D004372:Ducks / Q000378:metabolism*; D004734:Energy Metabolism; D005260:Female; D008297:Male; D009243:NAD / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption
D009243:NAD; D001285:Atropine