Metabolic Correction of Primary Hemostasis in the Acute Phase of Traumatic Brain Injury

The aim of the study was to investigate the effect of ethylmethylhydroxypyridine on the ultrastructural alterations in endothelial cells of liver sinusoidal capillaries (SC) and primary hemostasis in the acute phase of traumatic brain injury (TBI).Materials and methods. Ultrastructural endothelial cell changes were studied in 36 female outbred rats in the acute phase of TBI using electron microscopy, and the platelet count was determined using a blood analyzer. The experimental group (n=18) animals received intraperitoneal injections of ethylmethylhydroxypyridine at the dose of 8.0 mg/kg per day for 12 days, and the control group (n=18) rats were administered with normal saline solution at the same dose.Results. Administration of ethylmethylhydroxypyridine in the early post TBI period reduced microvilli damage in endothelial, hepatic and stellate cells in the Disse space, whereas in the control group a significant decrease of these cells counts was detected. In contrast to the control group, the experimental group animals did not demonstrate thrombocytopenia on the days 1, 3, and 7 after injury. There was a significant increase in the platelet count compared with the baseline values, which was highest on day 12 after injury.Conclusion. Intraperitoneal administration of ethylmethylhydroxypyridine in rats in early post TBI period inhibited the TBI-associated damaging effect of secondary factors on liver sinusoid endothelial cells and platelet consumption

LABOR PRODUCTIVITY AS A PRODUCTION EFFICIENCY FACTOR

El objetivo de esta investigación es estudiar el factor de eficiencia y la productividad laboral. En gran medida, el nivel de productividad laboral creció debido a la intensificación de la producción. Al mismo tiempo, según Rosstat, en agricultura, silvicultura y pesca solo hay un 8% de empleos altamente eficientes. Por lo tanto, el factor de intensificación de la producción se utiliza de manera insignificante. Es obvio que hay una necesidad de un componente innovador del crecimiento de la productividad laboral, por un lado, y la creación de nuevos empleos en las zonas rurales para los recursos laborales liberados, por otro lado. Aquí es necesario determinar los principales factores que afectan la productividad en las condiciones modernas, y justificar las propuestas para mejorarla.Of the goal of this investigation is to study the efficiency factor and labor productivity. To a large extent, the level of labor productivity grew due to the intensification of production. At the same time, according to Rosstat, in agriculture, forestry and fisheries there are only 8% of high-efficient jobs. Thus, the factor of production intensification is used insignificantly. It is obvious that there is a need for an innovative component of labor productivity growth on the one hand, and the creation of new jobs in rural areas for the released labor resources, on the other hand. Here it is necessary to determine the main factors affecting productivity in modern conditions, and to justify proposals to improve it.O objetivo desta investigação é estudar o fator de eficiência e a produtividade do trabalho. Em grande medida, o nível de produtividade do trabalho aumentou devido à intensificação da produção. Ao mesmo tempo, segundo Rosstat, na agricultura, silvicultura e pesca, existem apenas 8% dos empregos de alta eficiência. Assim, o fator de intensificação da produção é usado de forma insignificante. É óbvio que é necessário um componente inovador do crescimento da produtividade do trabalho, por um lado, e a criação de novos empregos nas áreas rurais para os recursos liberados, por outro. Aqui é necessário determinar os principais fatores que afetam a produtividade nas condições modernas e justificar propostas para melhorá- la

Метаболическая коррекция сосудисто-тромбоцитарного звена системы гемостаза в остром периоде черепно-мозговой травмы у крыс

The aim of the study was to investigate the effect of ethylmethylhydroxypyridine on the ultrastructural alterations in endothelial cells of liver sinusoidal capillaries (SC) and primary hemostasis in the acute phase of traumatic brain injury (TBI).Materials and methods. Ultrastructural endothelial cell changes were studied in 36 female outbred rats in the acute phase of TBI using electron microscopy, and the platelet count was determined using a blood analyzer. The experimental group (n=18) animals received intraperitoneal injections of ethylmethylhydroxypyridine at the dose of 8.0 mg/kg per day for 12 days, and the control group (n=18) rats were administered with normal saline solution at the same dose.Results. Administration of ethylmethylhydroxypyridine in the early post TBI period reduced microvilli damage in endothelial, hepatic and stellate cells in the Disse space, whereas in the control group a significant decrease of these cells counts was detected. In contrast to the control group, the experimental group animals did not demonstrate thrombocytopenia on the days 1, 3, and 7 after injury. There was a significant increase in the platelet count compared with the baseline values, which was highest on day 12 after injury.Conclusion. Intraperitoneal administration of ethylmethylhydroxypyridine in rats in early post TBI period inhibited the TBI-associated damaging effect of secondary factors on liver sinusoid endothelial cells and platelet consumption.Цель исследования — изучить влияние этилметилгидроксипиридина на ультраструктурные изменения эндотелиоцитов синусоидных капилляров (СК) печени и сосудисто-тромбоцитарное звено системы гемостаза в остром периоде черепно-мозговой травмы (ЧМТ).Материалы и методы. В посттравматическом периоде (ПТП) ЧМТ на 36 аутбредных крысах-самках исследовали динамику изменения ультраструктуры эндотелиоцитов СК печени методом электронной микроскопии и определяли количество тромбоцитов на гемоанализаторе. В течение 12 сут. в опытной группе (n=18) животным внутрибрюшинно вводили этилметилгидроксипиридин в дозе 8,0 мг/кг массы тела в сутки, а в контрольной группе (n=18) — физиологический раствор натрия хлорида в том же объеме.Результаты. Введение этилметилгидроксипиридина в ПТП уменьшало повреждение микроворсинок эндотелиоцитов, гепатоцитов и звездчатых ретикулоэндотелиоцитов в пространстве Диссе, тогда как в контрольной группе в этот период обнаруживали их выраженную редукцию. В отличие от контрольной группы, у животных опытной группы не выявили тромбоцитопению в 1-, 3- и 7-е сутки после травмы, отметили статистически значимое увеличение числа тромбоцитов, относительно исходных данных, достигшее наибольшей величины к 12-м суткам после травмы.Заключение. Внутрибрюшинное введение этилметилгидроксипиридина крысам в раннем ПТП сдерживало повреждающее действие формирующихся после ЧМТ вторичных факторов на эндотелиоциты синусоидов печени и потребление тромбоцитов

РОЛЬ ВТОРИЧНЫХ ФАКТОРОВ ПОВРЕЖДЕНИЯ МОЗГА В АКТИВАЦИИ СОСУДИСТОТРОМБОЦИТАРНОГО ГЕМОСТАЗА ПРИ ЧЕРЕПНОМОЗГОВОЙ ТРАВМЕ

Purpose of the study. To evaluate the role of secondary brain damage factors in activation of vascularplatelet hemostasis in traumatic brain injury (TBI).Material and methods. In the ICU, 30 patients with complex traumatic brain injury were examined and treated. In the posttraumatic period, in patient measurement of heart and vascular tone, platelets, hemoglobin, lactate, and active forms of oxygen in the blood were investigated.The study results have showed that damaged brain secondary factors accompanying concomitant TBI (circulatory insufficiency, hypoxia, acidosis and increased free radical formation) represent at the same time nonspecificstimuli for platelets and cells of blood vessels that consequently, cause systemic activation of the vascularplatelet link within the hemostasis system.Conclusion. Nonspecific systemic activation of the vascularplatelet hemostasis by secondary factors in the patients with concomitant TBI is one of pathogenetic components of ischemic brain damage.Цель исследования. Оценить роль вторичных факторов повреждения мозга в активации сосудисто-тромбоцитарного звена системы гемостаза при черепномозговой травме (ЧМТ).Материал и методы. В ОРиТ проведено обследование и лечение 30 пострадавших с сочетанной ЧМТ. В посттравматическом периоде у больных исследовали показатели сердечной деятельности и сосудистого тонуса, содержание тромбоцитов, гемоглобина, лактата и активных форм кислорода в крови.Результаты исследования показали, что сопровождающие сочетанную ЧМТ вторичные факторы повреждения мозга (недостаточность кровообращения, гипоксия, ацидоз и повышенное образование свободных радикалов) являются в то же время неспецифическими стимулами тромбоцитов и эндотелиоцитов кровеносных сосудов и, вследствие этого, вызывают системную активацию сосудистотромбоцитарного звена системы гемостаза.Заключение. Неспецифическая системная активация сосудистотромбоцитарного гемостаза вторичными факторами у больных при сочетанной ЧМТ является одним из патогенетических компонентов ишемического повреждения мозга

МОРФОЛОГИЧЕСКИЕ ИЗМЕНЕНИЯ В КРОВЕНОСНЫХ МИКРОСОСУДАХ МИОКАРДА ПРИ ЭКСПЕРИМЕНТАЛЬНОЙ ЧЕРЕПНОМОЗГОВОЙ ТРАВМЕ

Aim of the research is to evaluate the structure changes of the capillaries, arterioles, venules and intra and extravascular alterations in myocardium of rats after traumatic brain injury (TBI).Material and methods. Experiments were performed in 18 white male noninbred rats. Midline thoracotomy was performed, and the heart excised under intraperitoneal anesthesia (sodium thiopental) on 3, 7 and 12 days after TBI. Myocardial tissue of the left ventricle was examined under light and electron microscopy.The results showed that following brain trauma there were changes of microvascular wall characterized by alterations of permeability, paracellular oedema, outgrowths of vessel endothelium, swelling, edema, and thinning of endothelial cells, intussusceptions, vacuolization of cytoplasm with fragmentation within the myocardium of the rats with TBI. Intravascular changes were manifested by the formation of hyaline thrombi, microaggregates and sludge of red blood cells in the lumen, altered vascular membrane structures, bubbles or even complete absence of circulation in capillaries (noreflow). Alterations outside of the vascular wall were manifested by the formation of diapedetic hemorrhage and development of a strongly pronounced perivascular edema. The injury of microvessels and the microrelief of the luminal surface of endothelial cells appeared to be important factors of activation of vascularplatelet mechanism of hemostasis.Conclusion. Treatment of traumatic disease should consider the need in timely correction of nonspecific alter ations associated with TBI to optimize the restructuring of cytoskeleton of endothelial cells, abrogate endothelial dysfunction and prevent microcirculatory complications.Цель: оценить структурные изменения капилляров, артериол, венул, внутри и внесосудистые нарушения в миокарде крыс, перенесших черепномозговую травму (ЧМТ).Материал и методы. На 18 белых нелинейных крысахсамках моделировали ЧМТ. Через 3, 7 и 12 суток после травмы на фоне внутрибрюшинного введения тиопентала натрия осуществляли декапитацию крыс, производили срединную торакотомию и извлекали сердце. Ткань миокарда левого желудочка исследовали с помощью светового и электронного микроскопа.Результаты исследования показали, что у крыс, перенесших ЧМТ, в миокарде формируются изменения стенки микрососудов, которые проявляются в нарушении ее проницаемости, перицеллюлярном отеке, образовании выростов эндотелия в просвет сосуда, набухании, отеке, истончении и деформации поверхности эндотелиальных клеток, вакуализации и выбухании фрагментов цитоплазмы. Внутрисосудистые изменения проявляются образованием гиалиновых тромбов, микроагрегатов и сладжей, в обнаружении в просвете сосудов мембранных структур, пузырей и даже полного отсутствия циркуляции в части капилляров (феномен norefloy). Нарушения за пределами сосудистой стенки проявляются в формировании диапедезных кровоизлияний и развитии выраженного периваскулярного отека. Повреждения микрососудов и, особенно, микрорельефа люминальной поверхности эндотелиоцитов являются значимыми факторами активации сосудистотромбоцитарного звена системы гемостаза.Заключение. Терапия травматической болезни должна быть направлена на своевременную коррекцию патогенетических факторов, вызывающих перестройку цитоскелета эндотелиальных клеток, а также эндотелиальной дисфункции и нарушений микроциркуляции

The Role of Ozonized Erythrocytic Mass Transfusion in the Restoration of Myocardial Morphological Changes during Blood Loss (Experimental Study)

Purpose. To evaluate the role of ozonized erythrocytic mass transfusion in the restoration of damages in the architectonics of myocardium microvasculature and cardiomyocytes in case of a severe blood loss.Materials and Methods. Two batches of experiments were conducted, 17 white outbred rats in each. The animals were anesthetized with thiopental sodium (25 mg/kg). Blood loss was caused by taking 3ml of blood from the tail artery of rats, which is 35% of the circulating blood volume. One hour after the blood loss, transfusion of autoerythrocytes with normal saline solution and Ringer’s solution infusion in 1:1 ratio was performed in the control batch. In the experimental batch, 3 ml of autoerythrocytes treated with ozonized saline solution with ozone concentration of 2 mg/l and 3 ml of Ringer’s solution (1:1 ratio) were administered to rats. Erythrocyte mass was prepared from 3 ml of the autoblood harvested from the animals 3 days before the experiment. On a post-transfusion day5, in both batches and in five intact animals, hearts were removed following the intraperitoneal thiopental sodium injection (100 mg/kg). The left ventricle wall specimen from each heart was removed for examination. Histologic sections were stained with hematoxylin and eosin. The preparations were visually examined and morphometric studies were performed using microvisor Vizo-103.Results. It has been established that administration of ozonized erythrocyte for severe blood loss correction limited the decrease in numbers of capillary profiles and their diameters, formation of mixed and hyaline thrombi fully or partially occluding microvascular lumens, major hemorrhages and reduction of variation of nuclear profiles, decreased perivascular, pericellular, perinuclear, and endonuclear edema of myocardial tissue, cardiomyocyte overcontruction zone, and their ruptures.Conclusion. The positive trends for microcirculation indices, vascularization density and myocardial edematization as prognostic markers in assessing potential posthypoxic rehabilitation of damaged tissues upon blood loss correction with ozonized erythrocyte mass might be explained by the antihypoxic, antioxidant, and detoxifying actions of ozone on erythrocytes and/or its metabolites (ozonides) in the body post-transfusion

Morphological Changes in Myocardial Blood Microvessels in Experimental Craniocerebral Injury

Aim of the research is to evaluate the structure changes of the capillaries, arterioles, venules and intra and extravascular alterations in myocardium of rats after traumatic brain injury (TBI).Material and methods. Experiments were performed in 18 white male noninbred rats. Midline thoracotomy was performed, and the heart excised under intraperitoneal anesthesia (sodium thiopental) on 3, 7 and 12 days after TBI. Myocardial tissue of the left ventricle was examined under light and electron microscopy.The results showed that following brain trauma there were changes of microvascular wall characterized by alterations of permeability, paracellular oedema, outgrowths of vessel endothelium, swelling, edema, and thinning of endothelial cells, intussusceptions, vacuolization of cytoplasm with fragmentation within the myocardium of the rats with TBI. Intravascular changes were manifested by the formation of hyaline thrombi, microaggregates and sludge of red blood cells in the lumen, altered vascular membrane structures, bubbles or even complete absence of circulation in capillaries (noreflow). Alterations outside of the vascular wall were manifested by the formation of diapedetic hemorrhage and development of a strongly pronounced perivascular edema. The injury of microvessels and the microrelief of the luminal surface of endothelial cells appeared to be important factors of activation of vascularplatelet mechanism of hemostasis.Conclusion. Treatment of traumatic disease should consider the need in timely correction of nonspecific alter ations associated with TBI to optimize the restructuring of cytoskeleton of endothelial cells, abrogate endothelial dysfunction and prevent microcirculatory complications

THE RELATION OF SLEEP RESPIRATION DISORDERS AND CARDIOVASCULAR RISK

Aim. To assess the relation of obstructive sleep apnea syndrome (OSAS) by the data of Berlin questionnaire and risk of fatal cardiovascular events. Material and methods. Totally, 275 persons  studied (115 males, 160 females)  age  25-64 y.o., with unknown cardiovascular  complications, underwent structured  interview. The risk of sleep-disordered breathing was assessed by Berlin questionnaire, cardiovascular risk — by SCORE. Anthropometric  parameters  were  studied,   as  lipid profile,  fasting glucose, uric acid, creatinine, C-reactive protein, adiponectin, leptin. Results. The increased  OSAS risk according to Berlin questionnaire was found in 7,3% of the studies. Most (90,0%) common was concomitance of the  components   of OSAS such  as  snoring/stops of respiration  and cardiometabolic disorders. Males more frequently complained on snoring/ stops of breathing — 21,7% vs 6,3% (p=0,001), that determined  higher general risk of OSAS among them comparing to women — 11,3% vs 4,4% (p=0,03).  For males  (1,7%)  and  females  (3,1%)  the  complaints  on daytime sleepiness were less common. Among those 40 y.o. and older the increased  risk of OSAS was found in 9,8%, comparing to 1,2% younger than  40  y.o.  (p=0,01).  In higher  OSAS risk there  was  higher  total cholesterol  — 6,10±0,18  vs 5,53±0,09  mM/L (p=0,05) and low density lipoproteides — 4,17±0,19 vs 3,59±0,08 mM/L (p=0,02); they were more often overweight — body mass  index 31,73±1,19  vs 27,71±0,38  kg/m2 (p=0,001),   and   had   higher  systolic  pressure  —  134,89±4,96   vs 126,72±1,18  mmHg. (p=0,04) and diastolic pressure — 84,26±2,69  vs 78,55±0,80  mmHg (p=0,03).  Respondents with higher  risk of OSAS regardless the  gender,  did not differ by SCORE. While determine  the specific combinations of OSAS components, there was no independent significance of snoring/respiration  pauses  and daytime sleepiness  in the total cardiovascular risk by SCORE.Conclusion. In the Russian population, higher OSAS risk is associated with the signs of metabolic syndrome. Berlin questionnaire does not reveal the subgroups of those who have OSAS risk together with cardiovascular risk