| Summary: | Cerebral energy metabolism during apneic asphyxia and steady state hypoxia was compared in ducks and chickens; ducks tolerate apneic asphyxia 3-8 times longer than chickens. Fluctuations in the reduced form of respiratory chain nicotinamide
adenine dinucleotide (NADH) were monitored from the left cerebral hemisphere by a noninvasive fluorometric technique and used as an indicator of mitochondrial hypoxia. Electroencephalogram
(EEG) and surface PO₂ were recorded from the right hemisphere. Forced dives of 4-7 minutes 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, NADH fluorescence, and EEG) to those obtained in forced submergence of nonparalyzed ducks.
NADH fluorescence was expressed in arbitrary units (AU) where 100 AU was defined as the fluorescence change from normoxia to anoxia. After 1 minute of asphyxia NADH fluorescence in-creased by 37 AU ± 3.60 SEM (n = 54) in paralyzed chickens and 8 AU ± 1.41 SEM (n = 55) in paralyzed ducks. After 2 minutes the fluorescence increased by only 15 AU - 1.95 SEM in ducks. Both species showed an isoelectric EEG when fluorescence increased by approximately 35 AU indicating that anaerobic ATP production in ducks did not maintain brain function (EEG) for a greater accumulation of respiratory chain NADH. At a given decrease in tissue PO₂ ducks and chickens showed the same level of NADH increase indicating that both species are equally dependent on tissue PO₂ for the maintenance of redox state. Furthermore, the inhibition of cardiovascular adjustments by atropine in ducks caused NADH to increase faster during apneic asphyxia than in nonatropinized ducks. I conclude that the oxygen conserving cardiovascular adjustments are responsible for the increased cerebral tolerance to apneic asphyxia in ducks without any involvement of biochemical mechanisms. === Science, Faculty of === Zoology, Department of === Graduate
|
|---|
