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 hypoxia-tolerant 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.

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

Preface 1. Diving behavior 2. Challenges of the breath hold and the environment 3. Respiratory gas exchange 4. Oxygen storage and transport 5. Cardiovascular dive response 6. Adaptations in cardiovascular anatomy and hemodynamics 7. Muscle and locomotory work 8. Thermoregulation 9. Diving metabolism 10. The aerobic dive limit (ADL) 11. Pressure tolerance 12. Hypoxemic tolerance 13. Biomedical relevance References Index.

Diving Physiology of Marine Mammals and Seabirds

Ducks, fur seals, Weddell seals and probably most cetaceans seem to be able to dive and remain aerobic for durations that are consistent with their elevated stores of usable oxygen and their metabolic rate while diving being similar to that when they are resting at the surface of the water. Ducks, in fact, have a high metabolic rate while diving, mainly because of their large positive buoyancy, but other species have relatively low buoyancy, are better streamlined and use lift-based rather than drag-based propulsion. However, species such as the larger penguins, grey seals and elephant seals seem to achieve the impossible by performing a substantial proportion of their dives for periods longer than would be expected on the above assumptions, and yet remaining aerobic. The logical conclusion is that during such dives these species reduce their metabolic rate below the resting level (hypometabolism) and, in some of them, there is a regional reduction in body temperature (hypothermia) which may contribute to the reduction in metabolic rate.

Metabolic regulation in diving birds and mammals

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.510290407

Ischemia-reperfusion injury in rat fatty liver: role of nutritional status.

The Post-resuscitative and initial Utility in Life Saving Efforts (PULSE) Conference represented an initiative by leaders of the international scientific community who sought opportunities for major improvements in clinical outcomes after cardiopulmonary resuscitation and after resuscitation from serious traumatic injury.1 The experts focused on scientific research that would yield major advances in lifesaving care, including measurable increases in survival and functional recovery. However, unless research support is prioritized to address resuscitation, it is highly unlikely that these opportunities would soon be realized.

We lose more than 1000 lives each day in the United States from sudden, unexpected death, a fatality rate comparable to the crash of two 747 aircraft without survivors.2–5⇓⇓⇓ Cardiovascular disease is the leading cause of death among individuals aged greater than 65 years, the second leading cause of death among individuals aged 45 to 65 years, and the 5th leading cause of death among individuals aged 1 to 9 years.4,5⇓ Traumatic injuries in the United States were responsible for 147 891 deaths and 2.6 million hospitalizations, costing over $335 000 per death and resulting in 37 million emergency department visits in 1995.6,7⇓ Trauma is the leading cause of death among children and all individuals to age 34 years, the leading cause of loss of productive life-years of any disease, with societal costs (estimated by the National Safety Council) of $469 billion dollars annually, and the third leading cause of death among individuals aged 35 to 54 years. The Conferees anticipated that the availability of new intervention strategies with more effective diagnostic methodologies in the early post-injury time interval would not only save lives but also reduce morbidity.1 Accordingly, the PULSE participants cited current restraints and/or barriers to the delivery of more effective resuscitation interventions and reaffirmed that …

The PULSE Initiative Scientific Priorities and Strategic Planning for Resuscitation Research and Life Saving Therapies

During periods of O2 lack in liver of seals, mitochondrial respiration and adenosine triphosphate (ATP) synthesis are necessarily arrested. During such electron transfer system (ETS) arrest, the mitochondria are suspended in functionally protected states; upon resupplying O2 and adenosine diphosphate (ADP), coupled respiration and ATP synthesis can resume immediately, implying that mitochondrial electrochemical potentials required for ATP synthesis are preserved during ischemia. A similar situation occurs in the rest of the cell since ion gradients also seem to be maintained across the plasma membrane; with ion-specific channels seemingly relatively inactive, ion fluxes (e.g., K+ efflux and Ca++ influx) can be reduced, consequently reducing ATP expenditure for ion pumping. The need for making up energy shortfalls caused by ETS arrest is thus minimized, which is why anaerobic glycolysis can be held in low activity states (anaerobic ATP turnover rates being reduced in ischemia to less than 1/100 of typical normoxic rates in mammalian liver and to about 1/10 the rates expected during liver hypoperfusion in prolonged diving). As in many ectotherms, an interesting parallelism (channel arrest coupled with a proportionate metabolic arrest at the level of both glycolysis and the ETS) appears as the dominant hypoxia defense strategy in a hypoxia-tolerant mammalian organ.

Protective metabolic mechanisms during liver ischemia: transferable lessons from long-diving animals.

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Protective metabolic mechanisms during liver ischemia: transferable lessons from long-diving animals.