Cardiovascular Adjustments to Diving in Mammals and Birds

Blix, Arnoldus Schytte; Folkow, Björn

doi:10.1002/cphy.cp020325

Cited by 173 publications

(115 citation statements)

References 148 publications

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“…During diving, these animals rely on large endogenous stores of O 2 -either bound to hemoglobin in their blood or to myoglobin in their skeletal muscles -to support oxidative metabolic processes (Burns et al, 2007;Lenfant et al, 1970;Scholander, 1940). Such adaptations, along with cardiovascular and metabolic adjustments (Blix and Folkow, 1983;Folkow and Blix, 2010;Ponganis et al, 2011;Scholander, 1940), enable some seals and whales to remain submerged for a staggering 2 h (Hindell et al, 1991;Watkins et al, 1985). But towards the end of dives, arterial blood O 2 tension may still drop to only 12-20 mmHg, even during routine free diving (Meir et al, 2009;Qvist et al, 1986;Scholander, 1940), and encephalographic recordings made during simulated diving in seals have shown that cerebral integrity is maintained down to 7-10 mmHg (Elsner et al, 1970;.…”

Section: When the Brain Goes Diving: Adaptations For Hypoxia Tolerancmentioning

confidence: 99%

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

Larson

Drew

Folkow

et al. 2014

Journal of Experimental Biology

131

102

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Many vertebrates are challenged by either chronic or acute episodes of low oxygen availability in their natural environments. Brain function is especially vulnerable to the effects of hypoxia and can be irreversibly impaired by even brief periods of low oxygen supply. This review describes recent research on physiological mechanisms that have evolved in certain vertebrate species to cope with brain hypoxia. Four model systems are considered: freshwater turtles that can survive for months trapped in frozen-over lakes, arctic ground squirrels that respire at extremely low rates during winter hibernation, seals and whales that undertake breath-hold dives lasting minutes to hours, and naked mole-rats that live in crowded burrows completely underground for their entire lives. These species exhibit remarkable specializations of brain physiology that adapt them for acute or chronic episodes of hypoxia. These specializations may be reactive in nature, involving modifications to the catastrophic sequelae of oxygen deprivation that occur in non-tolerant species, or preparatory in nature, preventing the activation of those sequelae altogether. Better understanding of the mechanisms used by these hypoxiatolerant vertebrates will increase appreciation of how nervous systems are adapted for life in specific ecological niches as well as inform advances in therapy for neurological conditions such as stroke and epilepsy.KEY WORDS: Arctic ground squirrel, Cetacean, Hypoxia, Naked mole-rat, Seal, Turtle IntroductionEnvironmental conditions vary enormously for vertebrates, both with respect to the extreme conditions tolerated by a given species at different times and with respect to average living conditions tolerated by different species. Temperature is perhaps the most obvious example: from the poles to the equator, average ambient temperatures vary widely and have been accompanied by physiological adaptations appropriate to resident species; seasonal variations in temperature and resource variability can induce dramatic changes in physiological and/or behavioral patterns including migration and hibernation. Oxygen levels also vary widely, with animals adapted to sea level, high-altitude, underground and aquatic habitats. Oxygen levels can also change dramatically on a shorter-term basis, as can occur in tidal pools or in breath-hold divers. Approximately 20% of the oxygen consumed by the human body is used by the brain. The greater part of this oxygen is used to produce the ATP required to maintain the membrane potentials necessary for electrical signaling with synaptic and action potentials (Harris et al., 2012). In many vertebrates, including adult humans, interruption of the oxygen supply to the brain for more than a few minutes leads to irreversible neurological damage, including neuronal death. Without oxidative phosphorylation, ATP-dependent neuronal processes including ion transport and neurotransmitter reuptake decline sharply. Without pumping, ion gradients fail and neurons depolarize, releasing excessive levels...

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Section: When the Brain Goes Diving: Adaptations For Hypoxia Tolerancmentioning

confidence: 99%

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

Larson

Drew

Folkow

et al. 2014

Journal of Experimental Biology

131

102

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“…And since that time, diving physiologists have attempted to examine the nature of these physiological/metabolic/ biochemical responses in free-diving animals in order to better understand the mechanisms of hypoxemic (low oxygen) tolerance, ischemic (low blood flow) tolerance and pressure tolerance, as well as explore the physiological limits of the foraging behavior and ecology of these animals. The findings and hypotheses of this monograph have remained the core of diving physiology research, as evidenced in major reviews of diving physiology, both past and recent (Blix and Folkow, 1983;Butler and Jones, 1982;Butler and Jones, 1997;Elsner and Gooden, 1983;Kooyman, 1989;Kooyman and Ponganis, 1998;Ponganis, 2011;Ponganis et al, 2011;Ramirez et al, 2007;Zapol, 1996).…”

Section: After 73 Years Still the Foundation Of Diving Physiology Rementioning

confidence: 87%

After 73 Years, Still the Foundation of Diving Physiology Research

Ponganis

2013

Journal of Experimental Biology

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“…During diving, these animals rely on large endogenous stores of O 2 -either bound to hemoglobin in their blood or to myoglobin in their skeletal muscles -to support oxidative metabolic processes (Burns et al, 2007; Lenfant et al, 1970;Scholander, 1940). Such adaptations, along with cardiovascular and metabolic adjustments (Blix and Folkow, 1983;Folkow and Blix, 2010;Ponganis et al, 2011;Scholander, 1940), enable some seals and whales to remain submerged for a staggering 2 h (Hindell et al, 1991;Watkins et al, 1985). But towards the end of dives, arterial blood O 2 tension may still drop to only 12-20 mmHg, even during routine free diving (Meir et al, 2009;Qvist et al, 1986;Scholander, 1940), and encephalographic recordings made during simulated diving in seals have shown that cerebral integrity is maintained down to 7-10 mmHg (Elsner et al, 1970; Kerem and Elsner, 1973).…”

Section: When the Brain Goes Diving: Adaptations For Hypoxia Tolerancmentioning

confidence: 99%

Cellular Basis for Learning Impairment in Fragile X Syndrome

Larson¹

2014

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information , 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE August 2014 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Illinois at Chicago PERFORMING ORGANIZATION REPORT NUMBERChicago, IL 60612-4305 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThis research combines behavioral, electrophysiological, and molecular approaches to elucidate the cellular basis for learning impairment in Fragile X Syndrome (FXS), using olfactory learning in Fmr1-KO mice as a model system. We hypothesize that FMRP, the protein missing in FXS, participates in two aspects of circuit function that are critical to learning: synaptic plasticity and the generation and survival of new neurons in the adult brain. Efforts in the second year of support were directed toward establishing a method to specifically upregulate neurogenesis in adult fragile X mice, test fragile X mice for learning deficits in hippocampal-independent tasks, and determine if learning affects NMDA receptor trafficking to synapses. Significant advances have been made in the establishment of behavioral paradigms to test both hippocampal -dependent and -independent forms of olfactory learning. Experimental paradigms have also been refined for the study of neurogenesis in the olfactory bulb, glutamate receptor expression as it relates to olfactory learning in olfactory cortex and hippocampus, and the effects of aging on glutamate receptor expression. These studies are likely to advance our understanding of intellectual disability and autism in addition to the specific condition of fragile X syndrome. This knowledge will be necessary for the development of rational strategies for prevention and treatment of cognitive impairments from a variety of causes. SUBJECT TERMSFragile X Syndrome, synaptic plasticity, long-term potentiation, glutamate receptors, neurogenesis, olfactory learning INTRODUCTIONFragile X syndrome is the most common inherited form of intellect...

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Cardiovascular Adjustments to Diving in Mammals and Birds

Cited by 173 publications

References 148 publications

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

After 73 Years, Still the Foundation of Diving Physiology Research

Cellular Basis for Learning Impairment in Fragile X Syndrome

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