Key result
Diving bradycardia in ducks is driven by a nervous reflex from head submersion, hypercapnia, and anoxia, and can be simulated by mesencephalon stimulation.
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This study elucidates the physiological mechanisms of diving bradycardia in ducks, highlighting the roles of nervous reflexes, hypercapnia, anoxia, and specific brain regions.
The circulatory response in the “diving reflex” as indicated by changes in heart rate of unanesthetized ducks was found to depend on more than the asphyxia of submersion. “Diving” bradycardia was found to result from at least three factors; these were: I. A specific nervous reflex, resulting from submersion of the head. This first factor is the permissive and necessary factor for establishing the “diving reflex”, but it is strongly reinforced by at least two other mechanisms. II. The progressive hypercapnia during the asphyxia. III. The increasing anoxia during the asphyxia. The interrelationships of these three factors are briefly discussed. Stimulation of an area in the mesencephalon in many respects closely resembles the specific, central permissive factor needed for the “diving reflex”. A second area, in the diencephalon, was found from which cholinergic vasodilator fibers to the muscle vascular bed could be activated.
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Feigl et al. (1963) studied Diving reflex. Submersion and brain stimulation was evaluated on Changes in heart rate (bradycardia). Diving bradycardia in ducks is driven by a nervous reflex from head submersion, hypercapnia, and anoxia, and can be simulated by mesencephalon stimulation.
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