AJP - Regulatory, Integrative and Comparative Physiology, Vol 239, Issue 3 352-R357, Copyright © 1980 by American Physiological Society
Cerebral energy metabolism in mallard ducks during apneic asphyxia: the role of oxygen conservation
R. M. Bryan Jr and D. R. Jones
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.
