[Mithochondria signaling in adaptation to hypoxia].

A bioenergetic mechanism for development of urgent adaptation to hypoxia is considered. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compensatory activation of respiratory chain complex II is a major mechanism of urgent adaptation to hypoxia necessary for 1) succinate- related energy synthesis in conditions of oxygen deficiency and formation of urgent resistance in the body; 2) succinate- related stabilization of HIF-1alpha and initiation of its transcriptional activity related with formation of urgent and long-term adaptation; 3) succinate- related activation of a succinate-specific receptor GPR91.

[Phenotypic characteristics of factor expression induced by hypoxia and redox status of the rat neocortical cells at different stages of adaptation to hypoxia].

Hypoxic preconditioning induces two-phase increase of HIF-1alpha expression in the neocortex of low-resistance rats. The first, brief phase appears after each hypoxic episode and rapidly disappears in normoxic conditions. The second increase in of HIF-1alpha expression occurs in 24 hours after the hypoxic episode.

[Current issues of adaptation to hypoxia. Signal mechanisms and their role in system regulation].

A bioenergetic mechanism for development of urgent and long-term adaptation to hypoxia is considered. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compensatory activation of respiratory chain complex II is a major mechanism of urgent adaptation to hypoxia necessary for 1) succinate-related energy synthesis in conditions of oxygen deficiency and formation of urgent resistance in the body; 2) succinate-related stabilization of HIF-1alpha and initiation of its transcriptional activity related with formation of long-term adaptation; 3) succinate-related activation of a succinate-specific receptor CPR91.

[Energotropic, antihypoxic, and antioxidative effects of flavonoids].

Phytogenous flavonoid-containing agents (PFCA) are able to initiate electron flow bypassing the NAD-dependent region of respiratory chain, which is related with the activity of DT-diaphorase catalyzing two-electron reduction of quinones to hydroquinones and hydrogen peroxide in the presence of NADH and oxygen. This property is dramatically potentiated under the conditions of suppressed electron transport function of mitochondrial enzyme complex I (MEC I). In this process, part of the flow goes to the cytochrome region of respiratory chain and provides recovery of the MEC II and MEC III coupling function.

[The regulatory role of mitochondrial dysfunction in hypoxia and its interaction with transcription activity].

The mitochondrial respiratory chain participates in the performance of the signal system, which activates the realization of metabolic compensatory processes and coupled functional response to both single and repeated, long-term exposure to acute hypoxia. Under the conditions of reduced oxygen delivery to cells the mitochondrial respiratory chain is involved in the process of oxygen homeostasis regulation and modulates oxygen consumption, the rate of oxygen delivery from the extracellular milieu to mitochondria, and energy synthesis, activating hypoxia-specific transcription factors as well.

[Heart affection in patients with ankylosing spondiloarthritis].

Aim: To study features of heart disease in patients with alkylosing spondyloarthritis (ASA).

Material And Methods: We examined 56 ASA patients. Most of the examinees had spinal problems, moderate activity, x-ray sacroileitis stage III.

[Molecular mechanisms of tissue hypoxia and organism adaptation].

The mechanism for participation of aerobic energy metabolism in formation of urgent and long-term adaptation to hypoxia is under consideration. It is stated that changes in kinetic properties of mitochondrial enzyme complexes (MEC), primarily enzymes of the respiratory chain substrate region (MEC I), in response to oxygen shortage underlie diverse stages of bioenergetic (tissue) hypoxia. It was shown that economization of energy metabolism in adaptation to hypoxia occurs due to formation of a new mitochondrial population.

[Neurophysiological analysis of the effects of antihypoxic versus psychotropic agents].

The Fourie EEG spectral analysis of thr sensomotor cortex and dorsal hypocampus in freely moving rats could reveal the common pharmacological EEG effects of different antihypoxic agents (gutimin, amtizole, emoxipine, and 3-OPK). All the agents decreased the total EEG power (they all reduced the absolute power in all frequency bands) and simultaneously enhanced (2 relative power. The former suggests that there was a decrease in the energetic level of bioelectric fluctuations, which may indicate that the brain reduces its energetic functioning level.

[Effect of occlusive cerebral ischemia on functional status of the internal organs].

Biochemical parameters characterizing visceral functions were measured in the plasma of rats with brain ischemia induced by double occlusion of the carotid arteries. Functional insufficiency of the viscera is gradually forming in the course of occlusive ischemia of the brain. Functional insufficiency of the liver was observed in animals with severe neurological deficiency and subsequent lethal outcome.

[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.

[New approaches to designing metabolic antihypoxants].

The paper outlines a concept of recovering the energy-synthesizing dysfunction of the respiratory chain at different stages of hypoxia: at the early stage which shows the disturbances of mitochondrial enzymatic complex I function, their correction is made by using the redox agents shunting the transport of electrons at NADH-CoQ, as well as by means of different succinate-oxidase oxidation activators. At the later stages of hypoxia demonstrating the disturbances of electron transport function at the cytochrome site, their correction is effected by applying CoQ and cytochrome C. The mechanisms of the antihypoxic action produced by antioxidative agents are described.

[Nosogeny in "silent" myocardial ischemia].

Psychical reactions to ischemic cardiac disease (ICD) without angina pectoris in 29 patients with "silent" myocardial ishemia were investigated. It was demonstrated that both hypo- and hypernosognosias were observed in such patients. The former were presented by antihypochondria in individuals with hyperthymic or expansive schizoid personal features meanwhile the latter--by neurotic hypochondria in patients with hysterical characteristics.