Abstract
AbstractThe autonomic mechanisms controlling cardio‐vascular adjustments to diving have been studied in ducks using drugs which block adrenergic a‐receptors (phentolamine) or deplete catechol‐amine stores (reserpine). In animals thus treated there was a marked change in the cardiovascular reflex pattern upon diving. The vasoconstrictor response regularly seen in normal, submerged animals appeared to be abolished, and the diving bradycardia was only poorly developed. As a consequence, the treated animals had lost their capability to endure submersion for prolonged periods of time, the catecholamine depleter being more effective in this respect than the α‐receptor blocking agent. However, if noradrenaline was administered to a submerged animal pre‐treated with reserpine, peripheral vasoconstriction and bradycardia took place momentarily. It is concluded that the initial, quick slowing of the heart, which takes place upon submersion, results from an immediate parasympathetic activity associated with the reflex apnoea. The profound diving bradycardia gradually developing may be due to baroreceptor stimulation related to the peripheral vasoconstriction.
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