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How Do Marine Mammals Manage and Usually Avoid Gas Emboli Formation and Gas Embolic Pathology? Critical Clues From Studies of Wild Dolphins

Journal

FRONTIERS IN MARINE SCIENCE
Volume 8, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fmars.2021.598633

Keywords

diving physiology; lung function; dive response; plasticity; cardiac output; selective gas exchange hypothesis; gas embolic pathology; decompression sickness

Funding

  1. Office of Naval Research [N000141010159, N000141613088, N000141410563, N000140811220]
  2. ONR YIP Award [N000141410563]
  3. Dolphin Quest
  4. U.S. Department of Defense (DOD) [N000141613088] Funding Source: U.S. Department of Defense (DOD)

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Decompression theory based on terrestrial mammals may not apply to marine mammals, who are found to experience gas bubbles during diving. The bottlenose dolphin shows physiological or behavioral adaptations to prevent excessive uptake of N-2, potentially avoiding symptomatic gas emboli formation. Integral studies on cardiorespiratory function have enhanced the understanding of cetaceans' ability to dive to extreme depths.
Decompression theory has been mainly based on studies on terrestrial mammals, and may not translate well to marine mammals. However, evidence that marine mammals experience gas bubbles during diving is growing, causing concern that these bubbles may cause gas emboli pathology (GEP) under unusual circumstances. Marine mammal management, and usual avoidance, of gas emboli and GEP, or the bends, became a topic of intense scientific interest after sonar-exposed, mass stranded deep-diving whales were observed with gas bubbles. Theoretical models, based on our current understanding of diving physiology in cetaceans, predict that the tissue and blood N-2 levels in the bottlenose dolphin (Tursiops truncatus) are at levels that would result in severe DCS symptoms in similar sized terrestrial mammals. However, the dolphins appear to have physiological or behavioral mechanisms to avoid excessive blood N-2 levels, or may be more resistant to circulating bubbles through immunological/biochemical adaptations. Studies on behavior, anatomy and physiology of marine mammals have enhanced our understanding of the mechanisms that are thought to prevent excessive uptake of N-2. This has led to the selective gas exchange hypothesis, which provides a mechanism how stress-induced behavioral change may cause failure of the normal physiology, which results in excessive uptake of N-2, and in extreme cases may cause formation of symptomatic gas emboli. Studies on cardiorespiratory function have been integral to the development of this hypothesis, with work initially being conducted on excised tissues and cadavers, followed by studies on anesthetized animals or trained animals under human care. These studies enabled research on free-ranging common bottlenose dolphins in Sarasota Bay, FL, and off Bermuda, and have included work on the metabolic and cardiorespiratory physiology of both shallowand deep-diving dolphins and have been integral to better understand how cetaceans can dive to extreme depths, for long durations.

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