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53
гражданской обороны, медицинского университета
1. Определена положительная динамика изменений мезоморфного компонента соматотипа юношей-курсантов в течение обучения в училище гражданской обороны, тогда как другие компоненты уменьшались или оставались неизменными, что характеризует повышение атлетичности курсантов.
2. Выявлено незначительную отрицательную динамику изменений мезоморфного компонента соматотипа юношей-учеников на протяжении обучения
в училище гражданской обороны за счет перехода в экто-мезоморфы, характеризующая относительную грацилизацию учеников.
3. Выявлено отсутствие динамики изменений мезоморфного и эктоморфного компонентов соматотипа юношей-студентов в течение обучения в медицинском университете. Вместе с тем отмечается незначительное количественное перемещения внутри промежуточных типов соматотипа со стремлением к грацилизации студентов.
Список литературы:
1. Казакова Т. В. Конституциональные особенности физического статуса, вегетативной регуляции и метаболизма клеток иммунной системы в юношеском возрасте: автореферерат дис. ... д-ра мед. наук/Т. В. Казакова. - Красноярск, 2009. - 23 с.
2. Багнетова Е. А. Биоинформационный анализ факторов риска, влияющих на здоровье участников образовательного процесса в условиях ХМАО Югры: автореферат дис. ... д-ра биол. наук/Е. А. Багнетова. - Сургут; 2012. - С. 3-4.
3. Effect of activity and television viewing on BMI (body mass index) z-score in early adolescents in Turkey/E. N. Ozmert, R. Ozdemir, А. Pektas [et al.]//World J. of Pediatrics. - 2011. - Vol.7, - № 1. - P. 37-40.
4. Modern students in megapolis: morphofunctional features and lifestyle/V. Kuchma, N. Skoblina, N. Bokareva, O. Milushkina//Abstracts of the 4 European Conference on health promoting schools «Equity, Education and Health». - Odense, Denmark. - 2013. - P. 269-270.
5. Correlation between fat mass and blood pressure in healthy children/D. Drozdz, P. Kwinta, P. Korohoda [et al.]//Pediatr. Nephrol. - 2009. - № 9. - P. 35-40.
6. Мандриков В. Б. Соматотипологические и антропометрические особенности юношей допризывного возраста Волгоградского региона / В. Б. Мандриков, А. И. Краюшкин, А. С. Прачук//Вестник Волгоградского государственного медицинского университета. - 2011. - № 4. - С. 98-101.
7. Baltadjiev A. G./Somatotype characteristics offemale patients with type 2 diabetes mellitus/A. G. Baltadjiev//Folia Med (Plovdiv). - 2013 - Vol.55, - № 1. - P. 9-10.
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Indiaminov Sayit, Samarkand State Medical Institute, doctor degree in medicine, department of forensic medicine
E-mail: davolash@mail.ru
Damage to the brain in alcohol intoxication
Abstract: Analysis of contemporary condition concerning thanatogenetic study in alcohol intoxication and poisoning has been performed with selection of structural changes in the brain. It is emphasized that in brain structures in alcohol intoxication and poisoning the changes of cerebral vascular system and nervous elements are observed and that depends on ethanol concentration in blood and tissues, duration of its use, competitive conditions (diseases, trauma, etc.) The role ofvascular and nervous structures is shown according to the degree of pericellular and perivascular edema evidence in different sections of the brain in blood loss thanatogenesis on the background of alcoholemia.
Keywords: alcohol intoxication, brain changes, damage to hematoencephalic barrier.
Ethanol alcohol intoxication and poisoning hold stable leading place in fatal poisoning structure. Cases ofviolent and not violent death often occur on the background of alcohol intoxication and poisoning. There is a great number of works describing alcohol intoxication morphology (both acute and chronic) and acute alcohol intoxication in Forensic Medical literature [12; 28; 29; 30]. However at present there are not clear ideas concerning ethanol intoxication and poisoning specific signs and in this regard thanatogenesis is not clear in such conditions.
In order to reveal the possible death mechanisms in ethanol intoxication and poisoning the analysis of contemporary condition of the problem has been carried out taking into account the brain changes.
It is believed that ethanol intoxication has not any specific morphological signs [1]. However already early works emphasized the necessity ofpathomorphological study of the central nervous system in order to determine the cause of death due to ethanol alcohol intoxication [8]. At present many investigators are convinced of possible use of histomorphplogical signs in establishment of direct cause of death. Difficulty in alcohol intoxication morphological diagnostics is connected with multiformity of this process [26; 28]. In acute alcohol intoxication a person develops rough changes in the brain vascular system with disturbances of arterial and venous tonus, their overflowing with blood, plasmatic impregnation of their walls. Severe blood disturbances have been revealed and it results in formation of blood clots as well as in swelling, sludging and hemolysis of red blood cells. Extravascular manifestations of the brain circulation disturbances in persons with alcohol intoxication are presented as development of cerebral tissue edema and hemorrhagic syndrome. Nervous cells being in the condition of necrobiosis and necrosis are constantly revealed in different sections of the brain. The brain neurons and neuroglya in acute alcohol intoxication condition may be connected both by direct effect of ethanol and development ofsevere damages to cerebral hemocirculation. Combination of toxic and ischemic effect on the brain may cause the development of comparatively large foci of necrosis. The area of neuronic component reduces in the cortex and thalamus probably due to the death of some neurons. Specific neurocyte area does not reduce in the medulla but on the contrary it increases. Probably nervous cells in this vital section of the brain have great resistance to ethanol. They undergo dystrophic changes, however this process does not often result in their death [35; 37].
Many authors consider that typical manifestations of ethanol intoxication are metabolic disturbances and impairment of vascular wall permeability. In alco-
hol intoxication clearly marked brain edema as well as pia mater encephali edema with accumulation of large amount of fluid under it are often observed [1; 21]. Swelling and dystrophic changes of astrocytes, being in the content of hematoencephalic barrier, take place in the brain. Astrocytes transfer the main ethanol mass to cerebrospinal fluid. In repeated episodes of acute alcohol intoxication atrophic changes develop and grow in vascular endotheliocytes of microciculatory bed and pinocytosis decreases. In larger vessels arteriosclerosis and perivascular fibrosis develop. The foci of fibrinoid necrosis develop in arteriolar walls. Perivascular bleedings can take place. Damage to hematoencephalic barrier increases and astrocytes are destroyed due to constant hyperfunc-tion. Block at the astrocyte-neuron level develops, neu-trocytes undergo substrate and oxygen starvation with the following dystrophic changes that result in their partial death being the evidence of alcohol encephalopathy formation [23; 26]. Low single — doses of ethanol can cause vasodilatation, mediated by endothelium, whereas large doses destroy endothelial functions [20]. Potassium chloride has a definite role in alcohol effect on cerebral arterioles [16].
In ethanol intoxication marked vascular changes are revealed in the brain as a type of hyperemia, increased vascular permeability, stases in venules, peri-vascular and pericellular edema, diapedetic bleedings. Acute vascular changes are spread by diffusion but are predominantly marked in molecular layer of the large hemispheres, white substance and dentate nuclei zone of the medulla. Neurons appear to be swollen with chro-matolysis phenomena. A large number of "shadow" cells, decrease of specific neurons density are observed. Severity and spread of vascular and nervous cellular changes correspond each other [30; 34]. In morphological and morphometric study of the brain in corpses of persons with ethyl alcohol acute intoxication (ethanol content in blood and urine makes 4.1-8.9%) signs of damages to hypothalamus, medulla oblongata and pons with higher than 85-90% degree of damage and severity of damage making more than 20-30% of neurons have been revealed. In the black substance of the brain neurons depigmentation is determined in more than 2/3 field of vision. For acute alcohol intoxication combined cardiac- cerebral variant of thanatogenesis is typical. Morphological signs of slow death tempo have been revealed: predominance of ischemia and karyolysis of nervous cells over karyo and cytopicnosis, marked glyal reaction with considerable satellitosis and a large number of oligoglia, presence of pigment in gliocytes of the brain
black substance, dystrophic changes of ependymic layer with hulling of ependymocytes into intervillous space, hydration of villi of ventricular vascular plexus [4; 5]. In chronic alcoholism marked neuroglyal changes which do not disappear even in several years following discontinuation of alcohol are observed. People's alcoholism and chronic alcohol intoxication in animals are clearly marked in brain morphology. With this alcohol first of all damages the vessels, particularly those of microcicu-latory bed, that results in permeability increase of both the vessels and hemocephalic barrier producing severe damages to neurons and even their death. Hypoxia associated with hemodynamic disturbances contributes to such outcome [36; 38]. One of molecular mechanisms of alcoholism development associated with impairment of cerebral chromatin cells and histones modification has been revealed. It is supposed that endogenic systems of melanocortines modulate neurobiological responses to ethanol [24]. Ethanol metabolism can cause oxidation destruction of the brain metachondrial genome. In acute and continuous ethanol consumption morphometric parameters of neurons and neuroglia have been determined and they can be used as micromorphological diagnostic variant of alcohol intoxication its consequences and alcohol dependence [10; 11].
Morphology of hard drinking and alcoholism has both qualitative and quantitative difference. It is supposed that in hard drinking the damage to organs including the brain is caused by ethanol and in alcoholism depth and spread of morphological changes occur due to the action of its metabolite- acetaldehyde [24; 27]. The performed study on evaluation of activity of the main ethanol oxidizing enzymes in cerebral tissue in ethanol intoxication and in death from ischemic heart disease is the evidence of histological method expediency in evaluation of morphological manifestations in ethanol intoxication [6].
Alcohol is easily absorbed by brain tissue as a result of a large water content in it, high cerebral tissue vascu-larization and alcohol neutropy. The curve of alcohol content in the brain is often higher than in the blood and its location in the highest point is more than the highest alcohol content in the blood. Discharge of alcohol from the brain substance as well as from liquor is less than discharge from the other organs, tissues and blood. Decrease of alcohol content in liquor is the same as its decrease in the blood and in elimination phase it always remains higher than in the blood. In alcohol intoxication edema of the brain substance, hyperemia and edema of ventricular vascular plexus are noted. Increased
formation of cerebrospinal fluid in brain ventricles is observed. Alcohol passes through hematoencephalic barrier unobstractedly promoting the passage of a number of aminoacids. Together with alcohol concentration increase in the blood first of all large hemisphere cells then medulla oblongata and spinal cord cells respond to its presence [2].The problem concerning the role of neurochemical reactions in processes of tolerance and physical dependence on ethanol and in the mechanism of alcohol abstinence is difficult and promotes necessity to carry out numerous studies but it has not been solved as yet [32; 33]. Alcohol has potential effect on development of the brain edema, complicating the course of craniocerebral trauma [9].
Thanatogenesis evaluation in alcohol intoxication is of great complexity. There was made an effort to study enzymes taking part in exchange of ethanol in the brain. Three groups of neurons were marked out depending on presence and predominance of alcoholdehydrogenase and aldehyde dehydrogenase. Positive reaction on these enzymes was also marked in capillaries endothelium as they have a role of a barrier inhibiting the passage of excessive ethanol and acetaldehyde concentration into intercellular space ofthe brain. It is established that the time offatal outcome caused by alcohol cardiomyopathy corresponds to maximal alcohol content in cerebrospinal fluid but not in the blood. In the case of death caused by alcohol cardiomyopathy in elimination stage alcohol concentration in liquor was 29.3% higher than in the blood [24].
Experimental studies with acetylcholinesterase inhibition in rats prove central (and not peripheral) alcohol significance in hemodynamic disturbance in hemorrhagic shock [13].
The cause of death on the background of acute alcohol intoxication in a number of cases appears to be cardiac insufficiency as a result of damage to medulla oblongata centers with development of hypoxia and severe hemodynamic impairments [22].
In cases of intoxication caused by alcohol substitutes the development of cerebral thanatogenesis type was established as toxico- hypoxic damage to the trunk and death caused by respiratory center paralysis take place. Damages to the brain sections are differed by their irregularities: hyperchromia and karyopyknosis are observed in layer III, the most number of neurons with karyolysis and cytolysis are concentrated in layer V, marked neuronophagy is observed in layer VI. The most severe changes in the trunk are revealed in the large cells of reticular formation (sometimes almost 100% of neurons undergo acute karyolysis). With this changes
according to acute swelling type with the following cary-olysis and cytolysis predominated over ischemic ones. In motor neurons the changes are limited by swelling and nucleus ectopia. In small cells of vegetative and sensitive nuclei reversible dystrophic changes also predominate. If death is caused by combined intoxication of ethanol and its substitutes fibrin, hyaline and fibrinoerythrocytic clots are revealed in microcirculatory vessels with majority of their number being estimated in subcortical nuclei. Thus, in these conditions combined coagulopathic cerebral type of thanatogenesis takes place [7].
In fatal intoxications caused by alcohol substitutes the average level of cerebral hydration made 78.6±8.7%, whereas in acute ethanol intoxication it made 87.9±6.9%, i. e. the brain is less hydrated in alcohol substitutes intoxication than in ethanol intoxication. As for distribution of fluid on separate sections of the brain more marked hydration of the cortex in comparison with middle brain was noted in ethanol intoxication and in alcohol substitutes intoxication the reverse picture was observed. In the genesis of changes according to acute swelling and chromatolysis type with following death of cells the direct toxic effect of ethanol and the highest alcohols is probably of important role as inadequate severity of damage to the brain trunk neurons and the degree of microcirculatory vessels thrombosis development is noted. In the studied cases of poisoning cerebral type of thanatogenesis predominates [4].
The analysis of literature showed that in the brain structures in alcohol intoxication and poisoning the changes of various directions in cerebral vascular system and cerebral nervous elements are observed and it depends on ethanol concentration in the blood and tissues, duration of its consumption, competitive conditions (diseases, trauma, etc.). The problem of pathological conditions in acute alcohol intoxication and ethanol poisoning has not been solved yet. The cases of com-
bined pathology are particularly complex in this attitude when simultaneously with alcohol intoxication the signs of chronic diseases or traumas which can be the cause of death are revealed [7; 30]. The results of our study showed that in different variants of blood loss on the background of acute alcohol intoxication and acute alcohol poisoning the damage both to vessels and neurons is observed. Severity of damage to neurons, the size ofperi-cellular and perivascular edema is more significant in comparison with blood loss and shock without alcohol-emia [14; 20]. The received findings were confirmed by the following investigations [31]. We determined various role of vascular and nervous structures of the brain in blood loss thanatogenesis on the background of alcohol-emia by determining pericellular and perivascular edema correlation. The results showed that in acute blood loss on the background of acute alcohol intoxication perivascular edema predominated over pericellulal one in the hemispheric cortex and hypothalamus, of pericellular edema over perivascular one in medulla oblongata. In massive blood loss caused by disturbance of the heart and magistral vessels on the background of alcoholemia to 3% increase of marked perivascular edema degree in numerous brain sections takes place, whereas in peripheral vessels disturbance perivascular edema is marked in single injury but pericellular edema in plural injuries. In massive blood loss caused by disturbance of the heart and magistral vessels on the background of acute alcohol poisoning prevalence of pericellular edema takes place in all brain sections and in disturbance of peripheral vessels not the same degree of marked perivascular and peri-cellular edema is noted [20; 31]. Different role of the brain structures in thanatogenesis that we revealed in alcohol intoxication and poisoning on the background of various types of blood loss makes it possible to determine additional differential signs of forensic medical diagnostics of these conditions.
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A systematic method of research — the basis of modern diagnostics
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Ischenko Vitaliy, Professor Medicae, Pacific state medical University Vladivostok, E-mail: neurokib@mail Botvich Tatiana, candidate of biological Sciences, Pacific state medical University Vladivostok E-mail: botvichta@mail.ru Laruschkina Alla, candidate of medical Sciences, Pacific state medical University Vladivostok E-mail: alla.laryushkina@gmail.com
A systematic method of research — the basis of modern diagnostics
Abstract: The paper considers the diagnosis of internal organs diseases based on the spectroscopic analysis of brain bioelectrical activity. We have described a technology of recording and analysing brain rhythmic activity on the basis of induction magnetoencephalography. The main principles of functional and niveau
