80
Marine Mammal Physiology: Requisites for Ocean Living
However, we still know very little about why marine mammals are apparently unaffected by HPNS, and whether they possess specific neuroanatomical and physiological
adaptations to protect them. The mechanism of HPNS is currently unknown, but an opinion currently held by many researchers is that HPNS is caused by compression of the neural membranes. The compression is thought to change the structure and function of the
neural membranes, with secondary effects resulting in HPNS. The secondary effects could
involve changes in axonal conduction, synaptic transmission, or changes in the release
of neurotransmitters. Generally, membranes of the nervous system function over only a
small range of pressures—so, the deep-diving marine mammals are all the more remarkable for their tolerance to a high range of pressures.
Interestingly, anesthetic gases appear to ameliorate symptoms and provide increased
pressure tolerance in terrestrial mammals (Hunter and Bennett 1974). As N 2 behaves like
an anesthetic gas at elevated pressure, it has been suggested that high N 2 levels could
ameliorate HPNS symptoms. The myelin sheath is made up of lipids, and with a higher
solubility for N 2 in lipids, this might alter the “flexibility” for lipid chains at pressure,
allowing for more effective neurotransmission. Why marine mammals do not suffer from
the narcotic effect of N 2 is unknown, but the tissue PN 2 levels of deep-diving species may
be their primary way to avoid HPNS. The critical PN 2 for prevention of HPNS is less than
that causing N 2 narcosis in humans (Halsey 1982). So it is possible that regulation of N 2 is
to obtain levels sufficient to prevent HPNS but low enough to avoid N 2 narcosis.
4.2.6.2 Oxygen toxicity
In terrestrial mammals, there is a relationship between O 2 tension (PO 2 ), exposure time, and
O 2 toxicity (Harabin et al. 1995). During breath-holding, however, O 2 toxicity is unlikely to be
a problem as the PO 2 will only transiently reach high pressures and the continuous uptake of
O 2 will not last for an extended period of time (McDonald and Ponganis 2013; Qvist et al. 1986).
4.2.6.3 Decompression sickness
Theoretical modeling attempts have been made to estimate blood and tissue levels of N 2
(Fahlman et al. 2006; Houser et al. 2001; Zimmer and Tyack 2007), O 2 , and CO 2 (Fahlman
et al. 2007) in diving vertebrates. When combined with a refined description of Scholander’s
model of lung compression (Bostrom et al. 2008; Fitz-Clarke 2007) most model results suggest that accumulation of both N 2 and CO 2 may reach levels that would cause DCS symptoms in similar-sized terrestrial mammals (Fahlman et al. 2007, 2014b; Hooker et al. 2009,
2012; Kvadsheim et al. 2012).
Decompression sickness has been suggested as a potential explanation for lesions
coincident with intravascular and major organ gas emboli in beaked whales mass stranded
in conjunction with military exercises deploying sonar (Fernandez et al. 2005; Jepson
et al. 2003). There is some controversy about the proximate cause of gas emboli (Hooker
et al. 2012) although it is widely agreed that it appeared to be linked to anthropogenic
disturbance. These types of lesions have also been reported in some single-stranded cetaceans for which they do not appear to have been immediately fatal (Jepson et al. 2005).
Differences in N 2 solubility between species and between the body blubber and acoustic
fats may align with these observations (Koopman and Westgate 2012).
Osteonecrosis-type surface lesions have been reported in sperm whales (Moore and Early
2004). These were hypothesized to have been caused by repetitive formation of asymptomatic
N 2 emboli over time and suggest that sperm whales live with sub-lethal decompression-induced
bubbles on a regular basis, but with long-term impacts on bone health. However, experimental work using a captive bottlenose dolphin undergoing a dive schedule designed to induce
Marine Mammal Physiology: Requisites for Ocean Living
However, we still know very little about why marine mammals are apparently unaffected by HPNS, and whether they possess specific neuroanatomical and physiological
adaptations to protect them. The mechanism of HPNS is currently unknown, but an opinion currently held by many researchers is that HPNS is caused by compression of the neural membranes. The compression is thought to change the structure and function of the
neural membranes, with secondary effects resulting in HPNS. The secondary effects could
involve changes in axonal conduction, synaptic transmission, or changes in the release
of neurotransmitters. Generally, membranes of the nervous system function over only a
small range of pressures—so, the deep-diving marine mammals are all the more remarkable for their tolerance to a high range of pressures.
Interestingly, anesthetic gases appear to ameliorate symptoms and provide increased
pressure tolerance in terrestrial mammals (Hunter and Bennett 1974). As N 2 behaves like
an anesthetic gas at elevated pressure, it has been suggested that high N 2 levels could
ameliorate HPNS symptoms. The myelin sheath is made up of lipids, and with a higher
solubility for N 2 in lipids, this might alter the “flexibility” for lipid chains at pressure,
allowing for more effective neurotransmission. Why marine mammals do not suffer from
the narcotic effect of N 2 is unknown, but the tissue PN 2 levels of deep-diving species may
be their primary way to avoid HPNS. The critical PN 2 for prevention of HPNS is less than
that causing N 2 narcosis in humans (Halsey 1982). So it is possible that regulation of N 2 is
to obtain levels sufficient to prevent HPNS but low enough to avoid N 2 narcosis.
4.2.6.2 Oxygen toxicity
In terrestrial mammals, there is a relationship between O 2 tension (PO 2 ), exposure time, and
O 2 toxicity (Harabin et al. 1995). During breath-holding, however, O 2 toxicity is unlikely to be
a problem as the PO 2 will only transiently reach high pressures and the continuous uptake of
O 2 will not last for an extended period of time (McDonald and Ponganis 2013; Qvist et al. 1986).
4.2.6.3 Decompression sickness
Theoretical modeling attempts have been made to estimate blood and tissue levels of N 2
(Fahlman et al. 2006; Houser et al. 2001; Zimmer and Tyack 2007), O 2 , and CO 2 (Fahlman
et al. 2007) in diving vertebrates. When combined with a refined description of Scholander’s
model of lung compression (Bostrom et al. 2008; Fitz-Clarke 2007) most model results suggest that accumulation of both N 2 and CO 2 may reach levels that would cause DCS symptoms in similar-sized terrestrial mammals (Fahlman et al. 2007, 2014b; Hooker et al. 2009,
2012; Kvadsheim et al. 2012).
Decompression sickness has been suggested as a potential explanation for lesions
coincident with intravascular and major organ gas emboli in beaked whales mass stranded
in conjunction with military exercises deploying sonar (Fernandez et al. 2005; Jepson
et al. 2003). There is some controversy about the proximate cause of gas emboli (Hooker
et al. 2012) although it is widely agreed that it appeared to be linked to anthropogenic
disturbance. These types of lesions have also been reported in some single-stranded cetaceans for which they do not appear to have been immediately fatal (Jepson et al. 2005).
Differences in N 2 solubility between species and between the body blubber and acoustic
fats may align with these observations (Koopman and Westgate 2012).
Osteonecrosis-type surface lesions have been reported in sperm whales (Moore and Early
2004). These were hypothesized to have been caused by repetitive formation of asymptomatic
N 2 emboli over time and suggest that sperm whales live with sub-lethal decompression-induced
bubbles on a regular basis, but with long-term impacts on bone health. However, experimental work using a captive bottlenose dolphin undergoing a dive schedule designed to induce