1991
DOI: 10.1007/bf00839550
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Myocardial ultrastructure of rats differing in resistance to hypoxia, after acute and periodic exposure to it

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“…Long-term (LT) adaptation of animals to hypoxia has been shown to cause mitochondrial hyperplasia [4,15], activate protein synthesis [7,11], and raise mitochondrial cytochrome c [19] and cytochrome c oxidase levels [15] and the concentration of functional respiratory units [18] in the myocardium. Such changes may boost the power of the cardiac energysynthesizing system, reduce the ATP and creatine phosphate deficits in the cardiac tissue [7,13], and mitigate the damaging effects of hypoxia on the functional and metabolic homeostasis of cardiac cells.…”
Section: Abstract: Adaptation; Hypoxia; Cytochromes; Brain; Liver; Imentioning
confidence: 99%
“…Long-term (LT) adaptation of animals to hypoxia has been shown to cause mitochondrial hyperplasia [4,15], activate protein synthesis [7,11], and raise mitochondrial cytochrome c [19] and cytochrome c oxidase levels [15] and the concentration of functional respiratory units [18] in the myocardium. Such changes may boost the power of the cardiac energysynthesizing system, reduce the ATP and creatine phosphate deficits in the cardiac tissue [7,13], and mitigate the damaging effects of hypoxia on the functional and metabolic homeostasis of cardiac cells.…”
Section: Abstract: Adaptation; Hypoxia; Cytochromes; Brain; Liver; Imentioning
confidence: 99%