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

被引:19
作者
Fahlman, Andreas [1 ,2 ]
Moore, Michael J. [3 ]
Wells, Randall S. [4 ]
机构
[1] Global Diving Res Inc, Ottawa, ON, Canada
[2] Fdn Oceanog Comunitat Valenciana, Valencia, Spain
[3] Woods Hole Oceanog Inst, Biol Dept, Woods Hole, MA 02543 USA
[4] Mote Marine Lab, Chicago Zool Soc, Sarasota Dolphin Res Program, Sarasota, FL 34236 USA
关键词
diving physiology; lung function; dive response; plasticity; cardiac output; selective gas exchange hypothesis; gas embolic pathology; decompression sickness; DECOMPRESSION-SICKNESS RISK; DIVING WEDDELL SEALS; BOTTLE-NOSED WHALE; NEUTROPHIL ACTIVATION; METABOLIC-RATE; HEART-RATE; COMPLEMENT ACTIVATION; TURSIOPS-TRUNCATUS; BUBBLE FORMATION; PULMONARY-FUNCTION;
D O I
10.3389/fmars.2021.598633
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
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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页数:16
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