First aid kit for hypoxic survival: sensors and strategies.
Survival success under conditions of acute oxygen deprivation depends on efficiency of the central and peripheral chemoreception, optimization of oxygen extraction from the hypoxic environment and its delivery to the periphery, and adjustments of energy production and consumption. This article uses a comparative approach to assess the efficiency of adaptive strategies used by anoxia-tolerant and hypoxia-sensitive species to support survival during the first minutes to 1 h of oxygen deprivation. An aquatic environment is much more demanding in terms of diurnal and seasonal variations of the ambient oxygen availability from anoxia to hyperoxia than is an air environment. Therefore, fishes and aquatic turtles have developed a number of adaptive responses, which are lacking in most of the terrestrial mammals, to cope with these extreme conditions. These include efficient central and peripheral chemoreception, acute changes in respiratory rate and amplitude, and acute increase of the gas-exchange interface. A special set of adaptive mechanisms are engaged in reduction of the energy expenditure of the major oxygen-consuming organs: the brain and the heart. Both reduction of ATP consumption and a switch to alterative energy sources contribute to the maintenance of ATP and ion balance in hypoxia-tolerant animals. Hypoxia and hyperoxia are conditions favoring development of oxidative stress. Efficient protection from oxidation in anoxia-tolerant species includes reduction in the glutamate levels in the brain, stabilization of the mitochondrial function, and maintenance of nitric oxide production under conditions of oxygen deprivation. We give an overview of the current state of knowledge on some selected molecular and cellular acute adaptive mechanisms. These include the mechanisms of chemoreception in adult and neonatal mammals and in fishes, acute metabolic adaptive responses in the brain, and the role of nitrite in the preservation of heart function under hypoxic conditions.
López-Barneo
J
J
Universidad de Sevilla, Sevilla, Spain.
Nurse
C A
CA
Nilsson
G E
GE
Buck
L T
LT
Gassmann
M
M
Bogdanova
A Yu
AY
D000222:Adaptation, Physiological / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002344:Carotid Body / Q000502:physiology; D019439:Chromaffin Cells / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D000860:Hypoxia / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*; D013045:Species Specificity
D009573:Nitrites; D009569:Nitric Oxide; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D010100:Oxygen