期刊
BIOMEDICINES
卷 10, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines10092059
关键词
Adenosine; hypoxia; altitude; hyperoxia; diving
Exposure to extreme oxygen partial pressures can induce changes in the adenosinergic system, which play important roles in protecting the brain and lungs in high-altitude and deep-sea environments. Increased adenosine concentration helps protect the brain against hypoxia and is involved in the pathogenesis of mountain illness and neurological disorders. It also contributes to the prevention of high-altitude pulmonary edema and lung oxygen toxicity. On the other hand, decreased adenosine concentration during hyperoxic exposure leads to vasoconstriction and decreased cerebral blood flow, serving as a preventive measure against cerebral oxygen toxicity.
Climbers and aviators are exposed to severe hypoxia at high altitudes, whereas divers are exposed to hyperoxia at depth. The aim of this study was to report changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures. At high altitudes, the increased adenosine concentration contributes to brain protection against hypoxia through various mechanisms such as stimulation of glycogenolysis for ATP production, reduction in neuronal energy requirements, enhancement in 2,3-bisphosphoglycerate production, and increase in cerebral blood flow secondary to vasodilation of cerebral arteries. In the context of mountain illness, the increased level of A(2A)R expression leads to glial dysfunction through neuroinflammation and is involved in the pathogenesis of neurological disorders. Nonetheless, a high level of adenosine concentration can protect against high-altitude pulmonary edema via a decrease in pulmonary arterial pressure. The adenosinergic system is also involved in the acclimatization phenomenon induced by prolonged exposure to altitude hypoxia. During hyperoxic exposure, decreased extracellular adenosine and low A(2A) receptor expression contribute to vasoconstriction. The resulting decrease in cerebral blood flow is considered a preventive phenomenon against cerebral oxygen toxicity through the decrease in oxygen delivery to the brain. With regard to lung oxygen toxicity, hyperoxia leads to an increase in extracellular adenosine, which acts to preserve pulmonary barrier function. Changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures frequently have a benefit in decreasing the risk of adverse effects.
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