In this review, we have tried to summarize decompression theory based on studies on humans and land mammals that have allowed us to understand the physiological processes that may result in Gas Embolic Pathology (GEP) in marine mammals (and sea turtles). We then review the studies over the last 15 years that have investigated the the potential mechanism that result in GEP in during unusual events such as sonar exposure, and how this research has resulted in the Selective gas Exchange which explains how marine mammals can selective exchange oxygen and carbon dioxide without exchange of nitrogen and thereby maximize aerobic dive duration and also minimize the risk of the bends (see below for short video explaining this hypothesis).
If you have any questions, please do not hesitate to get in contact:
afahlman@whoi.eduTitle: How Do Marine Mammals Manage and Usually Avoid Gas Emboli Formation and Gas Embolic Pathology? Critical Clues From Studies of Wild Dolphins
Authors: Fahlman,A., Moore, M.J., Wells, R.S.
DOI:
10.3389/fmars.2021.598633URL:
https://www.frontiersin.org/article/10.3389/fmars.2021.598633Abstract: 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 generation of a
new hypothesis, the
selective gas exchange hypothesis, as to 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, participating voluntarily. These studies then 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 shallow- and deep-diving dolphins and have been integral to better
understand how cetaceans can dive to extreme depths, for long durations.
Explanation of the Selective Gas Exchange hypothesis: https://www.youtube.com/watch?v=sfBOpUuJv1c