[Present-day problems of hypoxia].
The basic mechanism of hypoxia is energy apparatus dysfunction which is associated with ensuing inactivation of mitochondrial enzyme complexes (from the substrate to terminal portion of the respiratory chain) in oxygen deficiency, which leads to impairments of aerobic energy synthesis, energy-dependent functions, metabolism, and structure of cells. The effects of hypoxia are realized by two ways: 1) by direct impact of oxygen deficiency on the cellular bioenergy apparatus, followed by its dysfunction (bioenergetic hypoxia); 2) by indirect impact via stressor activation of the neurohumoral link that leads to the trigger of a nonspecific cascade of functional and metabolic reactions, to impaired cell oxygen supply and delivery, which also ultimately favors the development of bioenergetic hypoxia. The sequence of bioenergetic impairments is the major mechanism of any forms of hypoxia and underlies the body's individual resistance to oxygen deficiency. To correct these disorders (to restore cell energy generation processes and to maintain them at the level sufficient to perform energy-dependent functions) is the main task of antihypoxic protection. In this connection, prognostic biochemical criteria of different stages of hypoxia have been developed; a new classification of antihypoxants by the mechanism of their action is proposed by identifying a group of specific energy metabolic correctors; a combined drug therapy policy in oxygen deficiency is substantiated by taking into account the body's phenotypic features.
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D000975:Antioxidants / Q000494:pharmacology; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000378:metabolism* / Q000517:prevention & control; D008928:Mitochondria / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology
D000975:Antioxidants