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9FORMS OF ADAPTATION TO HYPEROXIA
Savilov P.
Doctor of Medical Sciences, Professor, Anesthesiologist Tambov Central District Hospital, Tambov "The
laws of evolution of the organic nature of our planet are manifested by fundamental events - the adaptive and hereditary variability of living matter
(A. N. Leonov)
Abstract
This article examines the forms of adaptation to hypoxia (protective, adaptive and compensatory) proposed by the Soviet pathophysiologist A. N. Leonov. Examples of these forms are given and the mechanisms of their formation are analyzed. The role of oxygen in the appearance of the cell nucleus and mitochondria, the formation of the body's antioxidant defense, and the partial transfer of mitochondrial genes to the nuclear genome is shown. The mechanism of the negative chrono-and dromotropic effects of hyperoxia on the heart is described.
Keywords: hyperoxia, forms of adaptation, mitochondria, cell, heart, function
Now no one doubts that the first living formation on the earth was anoxybiotic, i.e. existed in an anoxic environment. In turn, photosynthetic oxygen-producing organisms appeared at the beginning of the Archean (more than 3.8 billion years ago) [1], but there was no oxygen in the atmosphere. This is due to the fact that throughout the Archean, oxygen was not accumulated in the atmosphere, but was quickly consumed for the oxidation of volcanic gases (hydrogen sulfide, sulfur dioxide, methane and hydrogen), as well as divalent iron compounds (Fe2+). Only at the turn of the Archean and Proterozoic did the flow of these gases into the atmosphere of the ancient Earth decrease as a result of the formation and stabilization of continental plates. As a result, the accumulation of oxygen in the atmosphere began. At the same time, its concentration was only 1% of the current [2]. It should be noted that during most of the Proterozoic period following the Archaean (2500 to 541.0 ± 1.0 million years ago), even periods of decreasing oxygen content in the atmosphere were observed. Despite this, the milestone of about 400 million years ago is associated with a rapid increase in atmospheric oxygen content [2]. From this it follows that "the evolutionary transition from an oxygen-free to an oxygen-free type of life was long and occurred through complex reactions of adaptation of the bio-organic nature to the increasing pressure of oxygen" [3]. With the gradual accumulation of oxygen in the atmosphere, each step of the evolution of living matter forward became a new stage of its adaptation to the increased content of atmospheric oxygen. Each subsequent period of development of the biosphere turned out to be hy-peroxic compared to the previous one. he improvement of aerobic adaptive processes and their formation occurred each time under new conditions with a higher concentration of oxygen, until its content in the atmosphere reached about 21% [3].
In the previous work [4], we considered the first position of the adaptive - metabolic theory of hyper-baric oxygen therapy by A. N. Leonov about hyperbaric
oxygen as a universal evolutionary adaptogen. Now we will analyze the second position of Leonov's theory, about the forms of adaptation to hyperoxia. It reads: The forms of adaptation-protective, adaptive (mobilizing action of HBO) and compensatory (substitutive action of HBO) - are determined by the oxidative and hyperbaric properties of oxygen under high pressure" [5].
The emergence and consolidation in the process of evolution of these forms of reaction of living organisms to super-saturation with oxygen was initially aimed both at protecting against the oxidative influence of oxygen, which acted as a pathogen for ancient prokary-otes, and at adapting ancient organisms to new conditions of existence. Fixed in the process of evolution, these forms of adaptation to super-saturation with oxygen predetermined the formation of three stages of adaptation (Table 1). They will certainly pass any organism that finds itself in conditions of super-saturation with oxygen [6]. However, the therapeutic effect of hyperbaric oxygen is associated with the adaptation stage, which should be the object of studying the mechanisms of hyperoxic sanogenesis. As for the toxic and terminal stages of adaptation to hyperoxia, its study is most interesting for specialists working in the field of diving and space medicine.
Turning to the characteristic of the protective stage of adaptation to hyperoxia, we note that its formation is based on the desire of a biological object to prevent or weaken the negative impact of hyperoxia on the body. So, if we proceed from the general biological role of oxygen as an evolutionary adaptogen, then it is legitimate to say [7] that one of the first protective forms of adaptation to hyperoxia was the formation of a shell around the DNA of an ancient prokaryote. Thus, the genome of the ancient prokaryote was protected from the influence of reactive oxygen species (ROS). Eventually, this led to the emergence of a cell nucleus and the transformation of an ancient prokaryotic cell into a eu-karyotic one.
Table
Stages of hyperoxic and posthyperoxic states according to A. N. Leonov [3]
Adaptation Toxic Terminal
The formation is based on functional, metabolic and morpho-genetic mechanisms Manifested by development: 1. Hyperoxic hypoxia 2. Neurotoxic seizures (P. Baer effect) 3. Pneumotoxic (L. Smith effect) Shock Collapse Death
Fig. 1 The assumed path of the evolutionary origin of mitochondria, taking into account the evolutionary saturation of the atmosphere with oxygen according to [7] with a change in.
Another example of a protective form of adaptation of the first unicellular organisms to survive in an oxygen environment was the absorption of an aerobic prokaryotic cell by ancient anaerobic eukaryotic cells with the formation of their endosymbiosis (Fig. 1). By penetrating the aerobic eukaryotic cell, the aerobic pro-karyotic cell isolated itself from the oxygen atmosphere. At the same time, the anaerobic eukaryote was able to use the aerobic prokaryote as an energy supplier for its own needs. This allowed eukaryotes at the beginning of their evolutionary path to switch from anaerobic to economically more profitable aerobic oxidation [7]. This example strengthens the evidence base of the symbiotic theory of the origin of mitochondria of modern eukaryotes [8]. In other words, the endosymbiosis of ancient eukaryotic anaerobic and ancient prokaryotic aerobic cells, caused by the need for their survival in new "oxygen-containing" conditions, led to the emergence and consolidation in the process of evolution of mitochondria, as a necessary component of eukaryotic cells.
The next example of a protective form of adaptation to hyperoxia, formed at the dawn of the emergence of aerobic life forms, is the transition of a part of the prokaryotic-endosymbiotic genes to the nucleus of the host cell-eukaryote [8]. Thus, the ancient prokaryotic cell, transferring part of its genome to the genome of the host cell, thus increased (mobilized) its survival in an oxygen environment, and, as a result, ensured its existence.
When describing the adaptive form of adaptation to hyperoxia, attention should be paid to the respiratory chain. Its formation in ancient cells is determined by the appearance of oxygen in the atmosphere, which turned out to be "an all-powerful converter, as if the architect, of the form and content of life on Earth" [5]. his has allowed the survival of ancient prokaryotes in the new (aerobic) conditions. On the other hand, their evolutionary transformation into mitochondria led to the fact that the formation of ROS in the course of its work took place in the hotel department of the eukaryote [9]. The nuclear genome of the host cell was not affected [7]. In turn, mitochondrial DNA, located near the mitochon-drial membrane, where respiratory chain enzymes are also localized, was able to "adapt" to the natural leakage of ROS. This resulted in the mandatory involvement of the mitochondrial genome in the reactions of hyperoxic adaptationogenesis, which increases the sanogenic potential of both the patient and the healthy organism [10].
In turn, the formation of ROS during the consumption of oxygen by ancient pro - and eukaryotes predetermined the formation of a multicomponent system of antioxidant protection. On the one hand, it maintained the concentration of oxygen radicals within the normal range, on the other hand, it regulated their formation under conditions of super-saturation with oxygen. There is every reason to talk about the different sensitivity of the mitochondrial and nuclear genome of the cell to the damaging effect of ROS, which damage the DNA of cell nuclei and cause chromosomal aberrations in them [11].
Unlike the genome of the cell nucleus, the mito-chondrial genome contains only 16,500 nucleotide pairs and encodes 2 ribosomal RNAs, 22 transport RNAs, and 12 different polypeptide chains [12,13]. In addition, mitochondrial DNA, unlike nuclear DNA, lacks both regulatory sequences and non-coding regions of the genome (introns). Each nucleotide in mitochondrial DNA is part of the coding sequence for either protein or RNA [12, 13]. Therefore, all DNA is transcribed in mitochondrial DNA, whereas only its individual genes are transcribed in the nucleus [14]. There is every reason to believe that this simplified transcription of DNA and RNA processing in mitochondria is a result of the adaptive adaptation of the genome of ancient aerobic prokaryotes to the constant formation of ROS during the absorption of oxygen from the atmosphere. It is impossible to exclude the phylogenetic formation of the dependence of mitochondrial endonucle-ases that cleave mitochondrial RNA on the intensity of free radical reactions in mitochondria associated with the activity of respiratory chain enzymes. From these positions, it is necessary to abandon the idea of the mi-tochondrial genome of eukaryotes as an evolutionary dead end [15].
If we analyze the effect of HBO on the activity of mitochondrial enzymes [16,17] expressed in both nuclear (glutamate dehydrogenase, GDH) and mitochon-drial (cytochrome oxidase,) genomes [18], we can draw the following conclusion. Hyperbaric oxygen can selectively affect not only the mitochondrial enzyme itself, but also the rate of its formation, determined by the expression of the corresponding gene of nuclear or mitochondrial DNA. The selective reaction of the GDG and cytochrome oxidase of the cell to hyperoxia, which depends, in particular, on its functional activity at the time of oxygenation, reflects the evolutionary nature of this phenomenon of adaptation of living matter to super-oxygen saturation. It cannot be excluded that the process of ROS influence on the expression of mito-chondrial DNA genes in HBO is, in particular, under the control of mitochondrial SOD, which catalyzes the neutralization of the superoxide anion, which is a natural "by-product" of the respiratory chain.
Protective and adaptive forms of adaptation to hy-peroxia are manifested not only morphogenetically, but also functionally: stimulation or inhibition of a physiological reaction (process, function). For example, a decrease in heart rate under HBO conditions, regardless of the state of heart activity at the time of oxygenation. The inhibitory effect of hyperoxia on the heart rate is based, among other things, on the direct effect of hy-perbaric oxygen on the conduction system of the heart (Fig.2). Another example is hyperoxic vasoconstriction of the arterioles of the large circulatory circle, one of the mechanisms of which is the activation of ROS formation in the mitochondria of vascular wall myocytes, which stimulate the release of signaling molecules. The latter increase the sensitivity of the postsynaptic membrane of myocytes to norepinephrine. At the same time, myocyte phosphorylase-C is activated, serotonin, endo-thelin, prostoglanlin F2 and H2 are synthesized, which together causes a contraction of the smooth muscle of the vascular wall [10].
The adaptive form of adaptation to hyperoxia is the basis of hyperoxic preconditioning, which is understood as an increase in the sanogenic potential of a healthy or sick organism caused by the use of therapeutic HBO regimens in the event of an expected impact on it of an emergency stimulus (pathogenic agent) [7,19]. Example 1. HBO (1.5 ata, 60 min, 2 sessions) before surgery prevents pathological bleeding during surgery due to the preventive elimination of platelet
dysfunction [20]. Example 2. HBO course (2-6 sessions of 1.8 ata, 20-38 min) in pregnant women with mitral stenosis before surgery, mitral commissurotomy reduced the risk of intraoperative complications [21]. Example 3. HBO (2.5 ata, 45-60 min, 3-4 sessions) before surgery for a posterior cranial fossa tumor prevented the development of postoperative tissue edema [22].
Figure 2 Mechanism of hyperoxic heart rate reduction. It is implemented through the guanylate cyclase system. HBO stimulates the release of acetylcholine, which interacts with M2-cholinergic receptors of the postsynaptic membrane to activate guanylate cyclase, through it, protein kinase-G is activated, which causes an increase in the output of K+ from the cells of the cardiac conduction system. The potassium current coming out of the cell inhibits slow diastolic depolarization, which leads to a decrease in conductivity and a decrease in heart rate. • - acetylcholine, ^=0- M2- cholinergic receptors, GuC - guanylate cyclase PK-G- protein kinase G.
Example 4. A course of HBO (1.5 ata, 40-60 min, 5-7 sessions) in patients with transient ischemic attacks reduces the risk of stroke [23]. Example 5. The use of HBO in the intervals between flights in pilots improves the quality of piloting, prevents the development of fatigue, reduces the severity of vegetative reactions when performing aerobatics by aviators [24]. Example 6. The HBO course before the flight increased the tolerance of overloads in the "head-pelvis" direction from 5 to 7 units without the use of any means of anti-overload protection [25]. Example 7. The course of HBO ( 0.15 MP, 50 min, 10 sessions) in the pre-season period of training hockey players increased the performance of athletes, especially in people with reduced resistance to oxygen deficiency [26].
The compensatory form of adaptation under hyperoxic exposure is primarily associated with the substitution action of HBO2, which is realized by two mechanisms: hyperbaric and oxidative. The hyperbaric mechanism of the replacement effect of hyperoxia is determined by an increase in the blood content of physically dissolved oxygen during the HBO session, which occurs in accordance with Henry's law. As a result, the
need for red blood cells "disappears". This has important sanogenic either in deficit ( e.g. hemorrhage), or a violation of their oxygen-transport properties (e.g. CO poisoning) [27].
The partial pressure of physically dissolved oxygen in arterial blood (PaO2) is about 100 mmHg, which is equivalent to about 3 ml O2/l ( 0.3 vol%). In venous blood, PaO2 is about 40 mmHg equivalent to 1.2 ml O2/l (0.12 vol%). Under conditions of oxygen respiration at a pressure of 1 ata, the saturation of arterial blood per set of physically dissolved oxygen increases by an average of 2 vol%. If 0.3 ml of O2 /100 ml of blood corresponds to PaO2= 100 mmHg, then 2 ml of O2 / 100 ml of blood is 640 mmHg. The amount of oxygen chemically bound to hemoglobin under HBO conditions increases slightly (by -0.6 vol%, up to -21 vol%), while the content of oxygen physically dissolved in arterial blood increases almost 7 times [5]. Based on calculations, it is assumed that in the conditions of HBO in the 3 ata (303.9 kPa) mode, the amount of physically dissolved oxygen in arterial blood increases to 6 vol%. If we take the arteriovenous oxygen difference of 5 vol% as the norm, then with HBO of 3
ata, the oxygen demand of cells is fully satisfied due to the fund of physically dissolved oxygen [28]. Calculations show that at 3 ata (303.9 kPa), the amount of physically dissolved oxygen in arterial blood increases to 6 vol%. If we take the arterio-venous difference in oxygen equal to 5 vol% as the norm, then with HBO in 3 ata, the consumption of oxygen by cells is completely satisfied by the fund of physically dissolved oxygen [5]. In other words, under HBO conditions, the main oxygen transporters from the lungs to the tissues are the extracellular sector of the blood, i.e. plasma. It is no coincidence that in conditions of dehydration, the therapeutic effect of HBO is manifested only after the preliminary elimination of hypovolemia with crystalloid solutions [29].
In the post-decompression period, the oxygenated organism undergoes rapid desaturation up to the development of posthyperoxic hypoxia and (or) posthy-peroxic hypoxemia [5,30]. It should be emphasized that identical hyperoxemia can compensate for the loss of 1/3 of the oxygen capacity of the blood, for example, in the acute period of massive bleeding. At the same time, in terms of the volume of circulating blood (about 3.5 liters), the reserve of physically dissolved oxygen increases by 35 times (up to 175 ml of O2). However, this amount of oxygen can not provide the metabolic needs of the human body for oxygen for one minute, even at rest. Therefore, hyperoxemia "should be perceived as a rapidly expending oxygen 'supply' during direct exposure to oxygen under high pressure" [5]. And no more!
As for the oxidative property of HBO2, it is based on the oxidative property of oxygen, which under HBO conditions changes depending on the state of the body at the time of oxygenation and is implemented through oxygen-dependent redox systems. Established in the process of evolution, these systems take part in the formation of the redox potential (RP), which is created on the main metabolic pathways: glycolysis, the electron transport chain of mitochondria and endoplasmic retic-ulum, the citric acid cycle and beta-oxidation of fatty acids [5,14]. The involvement of the nature, degree and sequence of these systems in hyperoxic adaptationo-genesis is important both for the manifestation of the therapeutic effect of hyperoxia and its toxic effect on the body. To date, three types (hyperbiotic, normobiotic and refractory) of ORP reactions to normobaric hy-peroxia have been identified in cells of the cerebral cortex and skeletal muscles, which determine the survival or death of animals with acute massive blood loss during a therapeutic HBO session [31,32]. An important element of the oxidative property of HBO2 is the involvement in hyperoxic adaptationogenesis of microso-mal oxidation and especially free radical processes, which play an important role in the formation of biological effects of HBO2 [33].
It would be naive to believe that the forms of adaptation to hyperoxia formed and fixed in the process of evolution are exclusively aimed at increasing the sanogenic potential of both healthy and sick organisms. Under certain conditions, some of them can provoke the development or intensification of pathological reactions. For example, a decrease in the respiratory rate during a HBO session associated with the depressing
effect of hyperbaric oxygen on the chemoreceptors of the carotid zone can lead to the development of hyper-capnia. If for a healthy person it passes, as a rule, without consequences, then, in the pathological syndrome of hypercapnic respiratory failure, the therapeutic effect of hyperbaric oxygen (with an incorrectly selected HBO mode) may be ineffective. In other words, it is one of the examples of the manifestation of Hegel's law of unity and struggle of opposites, applied to the interaction of a living organism with a hyperoxic environment and its behavior in the post-hyperoxic period.
In this article, we will focus only on some examples of forms of adaptation to hyperoxia. Naturally, they can be cited much more. It should be noted that the forms of adaptation to hyperoxia can also have a non-evolutionary origin, and develop in the body depending on both the state of its functional-metabolic and moro-phgenetic systems at the time of oxygenation, and HBO regimes. For example, the different reaction of the glu-tamine cycle of hepatocytes of healthy and regenerating liver to HBO in the therapeutic mode [34,35,36], or the reaction of the antioxidant systems and lipid peroxidation of the brain [37] and lung structures [38] to a different number of HBO sessions.
A recent increase in telomere length in skin cells after a course (within one and a half months) of HBO use, detected in healthy volunteers, is of particular interest [39]. This is another clear example of adaptation to long-term periodic exposure to HBO in a therapeutic mode, which is most likely adaptive in nature. elomeres are the end sections of chromosomes that are characterized by a lack of ability to connect to other chromosomes or their fragments and perform a protective function. Elongation of telomeres extends the life of cells [40]. If we take into account that telomerase is responsible for this process [41], then there is every reason to talk about the effect of long-term use of HBO on the activity of this enzyme, which, depending on the stage of the cell cycle at the time of hyperkoxic exposure, as well as the number of HBO sessions, is likely to be of a regulatory nature. that is, either inhibit or stimulate this enzyme. At the same time, the refractoriness of telomerase of individual cells to certain HBO regimens is not excluded. One of the reasons for the lack of resumption of neoplastic processes in the bone marrow after the use of HBO to eliminate the side effects of chemotherapy in patients with leukemia [42] is probably a change in the hyperbaric oxygen activity of telomerase in cancer cells that survived but were weakened by the action of antitumor drugs. There is evidence that te-lomerase, depending on the type of cell, can take part in both the "immortality" of cancer cells [43] and, conversely , inhibit their growth, in particular, preventing chromosome fragmentation [44].
Conclusion. We have not analyzed all the examples of forms of adaptation of a healthy and sick body to hyperoxia. Some of these forms were formed and fixed in the process of a long evolutionary transition from anaerobic to aerobic life, while others are manifested in modern conditions depending on the state of the body at the time of oxygenation and the magnitude of hyperoxic load. The study of these, as well as the discovery of new forms of adaptation to hyperoxia, will
significantly expand the possibilities of using hyperbaric oxygen for both therapeutic and preventive purposes.
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POSSIBILITIES OF MULTISPIRAL COMPUTED TOMOGRAPHY IN THE DIAGNOSIS OF CORONARY CALCIFICATION IN PATIENTS WITH DYSPLASTIC HEART
Pimenov L.
Doctor of medical sciences, professor, head of the Department of General Practice and Internal Medicine with the Course of Emergency Medicine, Izhevsk State Medical Academy, Izhevsk, Russia
Remnyakov V.
Candidate of medical sciences, radiologist, head of the Department of Computed Tomography, Republican
Clinic and Diagnostics Center, Izhevsk, Russian Federation
Smetanin M.
Candidate of medical sciences, sonographer, radiologist, Republican Clinic and Diagnostics Center,
Izhevsk, Russian Federation
Avdeev AE.
Radiologist, Republican Clinic and Diagnostics Center, Izhevsk, Russian Federation
Chernyshova T.
Doctor of medical sciences, professor of the Department of General Practice and Internal Medicine with the Course of Emergency Medicine, Izhevsk State Medical Academy, Izhevsk, Russia
Abstract
The problem of heart connective tissue dysplasia syndrome is extremely relevant due to the increased risk of rhythm and conduction disorders, infectious endocarditis, thromboembolism and sudden cardiac death (SCD). Structural heart diseases (SHD) are manifestations of small anomalies of development on the part of the cardiovascular system. Dysplastic heart refers to the combination of constitutional, topographical, anatomical, and functional features of the heart in a patient with connective tissue dysplasia (CTD). The standard for the diagnosis of coronary calcification (CC), one of the known predictors of coronary heart disease (CHD) and complications of cardiovascular diseases (CVD), is multispiral computed tomographic scanner (MSCT).
Keywords: women, connective tissue dysplasia, structural heart diseases, coronary calcification, multispiral computed tomography, ECG synchronization.
