Cerebral energy metabolism in diving and non‐diving birds during hypoxia and apnoeic asphyxia.

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Abstract
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 NADH were monitored from the left cerebral hemisphere by a non-invasive fluorometric technique and used as an indicator of mitochondrial hypoxia. NADH fluorescence was expressed in arbitrary units (a.u.) where 100 a.u. was defined as the fluorescence change from normoxia to anoxia. EEG and surface PO2 [O2 partial pressure] were recorded from the right hemisphere. After 1 min of asphyxia, NADH fluorescence increased by 37 a.u. .+-. 3.60 S.E. [standard error] of mean (n[number] = 54) in paralyzed chickens and 8 a.u. .+-. 1.41 (n = 55) in paalyzed ducks. After 2 min the fluorescence increased by 15 a.u. .+-. 1.95 in ducks. Both species showed an isoelectric EEG when fluorescence increased by approximately 35 a.u., 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. Biochemical adjustments which enhance anaerobic ATP production and/or prolong oxidative phosphorylation during progressive hypoxia are not responsible for increased cerebral tolerance to apneic asphyxia in the duck.