[MARMAM] A new hypothesis how stress may alter physiology and diving related trauma

Andreas afahlman at whoi.edu
Wed Apr 25 01:32:38 PDT 2018

My co-authors and I are pleased to share our recently published article:

García-Párraga, D., Moore, M. and Fahlman, A. (2018). Pulmonary ventilation– perfusion mismatch: a novel hypothesis for how diving vertebrates may avoid the bends. Proceedings Royal Society B 285: p. 20180482-2018048.

This article is open access and copies can be downloaded at: http://rspb.royalsocietypublishing.org/content/285/1877/20180482 <http://rspb.royalsocietypublishing.org/content/285/1877/20180482>  For further information, please contact afahlman at whoi.edu. 

How some marine mammals and turtles can repeatedly dive as deep and long as they do has perplexed scientists for a very long time. This review opens a new window through which we can take a new perspective on the question

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air breathing marine vertebrates may, under unusual circumstances, develop gas emboli that result in decompression sickness (DCS) symptoms. Theoretical modeling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modeling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N2 levels that would result in severe DCS severe symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation (V) and cardiac output/lung perfusion (Q), varying the level of V/Q in different regions of the lung. Man-made disturbances, causing stress, could alter the V/Q  mismatch level in the lung, resulting in an abnormally elevated uptake of N2, increasing the risk for gas emboli. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing gas emboli, and provides a new mechanism for how marine vertebrates usually avoid the diving related problems observed in human divers.

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