Abstract
In many vertebrate types, including man, changes in the heart and circulation are brought about during breath-hold diving, which include bradycardia, selective peripheral vasoconstriction and a reduction in cardiac output. The mean arterial blood pressure, however, remains relatively unaltered [see reviews by Eisner (1) and Angell-James and Daly (2)]. These changes provide a defence mechanism against asphyxia whereby the oxygen stores of the body are conserved by diversion of the reduced cardiac output through those tissues of the body, brain and heart, which are essential for survival and are least able to withstand periods of prolonged hypoxia. These cardiovascular adaptations are more prominent in marine than in terrestrial mammals, so that the harbour seal, for instance, can remain submerged for up to 25 min. Nevertheless towards the end of its dive the arterial Po2 and Pco2 reach levels (10 and 100 mmHg, respectively) beyond those that can be tolerated by terrestrial mammals (3). It follows that the vigorous respiratory drive which chemical stimuli of this magnitude produce in the spontaneously breathing non-diving seal must be suppressed during diving (4).
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de Burgh Daly, M., Angell-James, J.E., Elsner, R. (1980). Cardiovascular-Respiratory Interactions in Breath-Hold Diving. In: Koepchen, H.P., Hilton, S.M., Trzebski, A. (eds) Central Interaction Between Respiratory and Cardiovascular Control Systems. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67603-1_26
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DOI: https://doi.org/10.1007/978-3-642-67603-1_26
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