scholarly journals VASCULAR PLEXUS AND BRAIN MICROCIRCULATION IN HIGH ALTITUDE CRANIOCEREBRAL INJURY

Author(s):  
M.S. Shuvalova ◽  
A.S. Shanazarov ◽  
Yu.Kh.-M. Shidakov

Mountains occupy about 24 % of the land surface. There are significant natural resources here, the development of which is associated with an increased traumatic risk. Craniocerebral injuries in the mountains are very frequent, and microvascular dysfunction, as under ordinary conditions, is a key element in the chain of events in the central nervous system. However, there are very few data on vascular plexuses and brain microcirculation in craniocerebral injury that occurs in the mountains. The aim of the study is to reveal the patterns in remodeling of vascular plexuse and main elements of brain microcirculation in craniocerebral injury that occurs in the mountains. Materials and Methods. The study enrolled 46 white outbred male laboratory rats (210–270 g) with simulated low-mountain (760 m above sea level, Bishkek) and high- mountains (Too Ashuu mountain pass, 3200 m above sea level) traumatic brain injury. The authors used the weight-drop method (Y. Tang technique) to reproduce the traumatic brain injury. After reproduction of the trauma in high altitudes, the animals were transported to low altitudes and on the 3rd day the rats were sacrificed with chloroform overdose. The authors studied microcirculation using a microscopic method with black ink intravascular injection. Olympus Bx40 microscope (Japan) was used for this purpose. At the same time, serial microphotography with simultaneous recording of the results was carried out using a digital camera connected to a computer. The morphometry of the vascular plexuse brain components was carried out with Top View application used for measuring microscopic objects. SPSS 16.0 software was used to process statistical data. Results. Craniocerebral injury that occurs in high mountains causes the narrowing of the capillary lumen by 52 % (p<0.001). In comparison with low mountains, the capillary lumen in high mountains decreases by 42 % (p<0.001). Venous plethora is observed. In vascular plexuses in the highlands, remodeling of the cellular component is recorded: ependymocyte volume increases by 23 % (p<0.05), nucleus volume – by 30 % (p<0.001), and cytoplasm volume – by 22 % (p<0.05). Conclusion. Craniocerebral injury leads to the development of cytotoxic edema in the vascular plexus stroma and to remodeling of brain microcirculation, which is the pathogenetic basis for hypertension and increased intracranial pressure. In the highlands, these phenomena are more pronounced and are accompanied by blood flow centralization. Keywords: microcirculation, vascular plexuses, brain, craniocerebral injury, highlands. Горы занимают около 24 % территории суши. Здесь располагаются значительные природные ресурсы, освоение которых сопряжено с повышенным риском травматизма. Черепно-мозговая травма на горных высотах – частое явление, а микрососудистая дисфункция, как и в обычных условиях обитания человека, является ключевым звеном в цепи событий, развертывающихся в центральной нервной системе. Однако данных о состоянии сосудистых сплетений и микроциркуляции головного мозга при черепно-мозговой травме, возникшей в высокогорье, крайне мало. Цель исследования – выявить закономерности ремоделирования сосудистых сплетений и основных звеньев микроциркуляции головного мозга при черепно-мозговой травме, возникшей в условиях высокогорья. Материалы и методы. Объектом исследования послужили 46 белых беспородных лабораторных крыс-самцов весом 210–270 г, которым моделировалась черепно-мозговая травма в условиях низкогорья (высота 760 м над уровнем моря, г. Бишкек) и высокогорья (перевал Туя-Ашу, 3200 м над уровнем моря). Для воспроизведения черепно-мозговой травмы использовалась ударная модель weight drop method по Y. Tang. После воспроизведения травмы в условиях высокогорья животных транспортировали в условия низкогорья и на 3-и сут выводили из эксперимента путем передозировки хлороформа. Микроциркуляция изучалась микроскопическим методом с применением внутрисосудистого инъецирования раствором черной туши. Препараты изучались под микроскопом Olympus Bx40 (Япония). Параллельно проводилось серийное микрофотографирование с помощью цифрового фотоаппарата, подключенного к компьютеру, с одновременным протоколированием результатов. Морфометрия компонентов сосудистых сплетений головного мозга осуществлялась с помощью приложения для измерения микроскопических объектов Top View. Статистическая обработка данных проводилась в программе SPSS 16.0. Результаты. Черепно-мозговая травма, возникшая в условиях высокогорья, приводит к сужению просвета капилляров на 52 % (p<0,001), при этом в сравнении с низкогорьем просвет капилляров в высокогорье уменьшается на 42 % (p<0,001). Отмечаются явления венозного полнокровия. Со стороны сосудистых сплетений в высокогорье регистрируется ремоделирование клеточного компонента: объем эпендимоцитов возрастает на 23 % (p<0,05), объем ядра – на 30 % (p<0,001), объем цитоплазмы – на 22 % (p<0,05). Выводы. Черепно-мозговая травма привела к развитию цитотоксического отека стромы сосудистого сплетения и ремоделированию системы микроциркуляции головного мозга, что является патогенетической основой гипертензии и повышения внутричерепного давления. В высокогорье эти явления выражены в большей степени и сопровождаются признаками централизации кровообращения. Ключевые слова: микроциркуляция, сосудистые сплетения, головной мозг, черепно-мозговая травма, высокогорье.

2007 ◽  
Vol 35 (5) ◽  
pp. 644-656 ◽  
Author(s):  
D Feng ◽  
W Xu ◽  
G Chen ◽  
C Hang ◽  
H Gao ◽  
...  

Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes and apoptosis in the intestine. Glutamine has been shown to reduce bacterial translocation and maintain intestine mucosal integrity, but its effects on the inflammatory response, structural alterations and apoptosis in intestinal mucosa following TBI have not been previously investigated. Using the weight-drop method, a right parietal cortical contusion was induced in rats and, for the next 5 days, they were fed either chow alone or chow mixed with glutamine. Intestinal tissue samples were then removed for analysis. Following TBI, glutamine supplementation was found to: decrease intestinal concentrations of interleukin (IL) −1β, tumour necrosis factor-α (TNF-α) and IL-6; downregulate intercellular adhesion molecule-1 (ICAM-1) expression; attenuate TBI-induced damage to the intestine structure; and reduce apoptosis. These results suggest that post-TBI glutamine administration could suppress intestinal inflammation, protect intestinal mucosal structure and reduce mucosal apoptosis.


2020 ◽  
Author(s):  
Wenhe Li ◽  
Haijun Zhu ◽  
Yue Liang ◽  
Fang Tong ◽  
Yiwu Zhou

Abstract Background: Biomarkers play an important role in accurate diagnosis of traumatic brain injury (TBI). Due to the complexity and diversity of TBI, it is likely that a single biomarker will not be used for exactly diagnose. Amyloid-beta (Aβ) protein is generated by sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase, which may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain as damage factor of TBI. Its use in diagnosis for TBI is becoming more widespread. Neuroglobin (NGB) protein is great potential to diminish neuronal damage. Most epidemiological evidence suggested that Aβ and NGB may be used as biomarkers on brainstem (BS) following TBI. The aim of this study was to investigate the trend of Aβ and NGB on BS of rats with TBI and to analyze comprehensively them as potential biomarkers. Methods: Adult male Sprague-Dawley rats were subjected to the modified weight-drop model of closed TBI. Biologic behavior observation, histopathological assessments and western blot assay were performed. Aβ and NGB expression indicated temporal changes in BS after TBI. Their accuracy and efficiency of performing these tasks were calculated and statistical comparisons performed.Results: The results of Aβ enable us to speculate that the time points of 3 h, 6 h and 12 h may be crucial points for the diagnosis of TBI. NGB expression in the injured had obvious difference versus the control, the points of 1 h and 3 h were apparently higher than the control, and the groups of 12 h and 48 h were two peaks in the present study. Furthermore, the immunofluorescence assay results supported that Aβ and NGB co-localization in the neuros of BS, and the NGB specific expression in the BS of neurons.Conclusions: Therefore, the expression and change rules of Aβ and NBG in the BS may provide an important foundation for the diagnosis of TBI, damage assessment and therapeutic intervention.


2016 ◽  
Vol 33 (13) ◽  
pp. 1171-1180 ◽  
Author(s):  
Fabian Büchele ◽  
Marta M. Morawska ◽  
Sebastian R. Schreglmann ◽  
Marco Penner ◽  
Markus Muser ◽  
...  

2021 ◽  
Vol 7 (9) ◽  
pp. 360-374
Author(s):  
M. Shuvalova ◽  
Yu. Shidakov ◽  
D. Zhanuzakov ◽  
A. Mamytova

Today, the traumatic epidemic is gaining momentum around the world. Having a complex pathogenesis, many aspects of the development and impact of traumatic brain injury (TBI) on the body remain undescribed. In particular, there is practically no information about the state of the body after a traumatic brain injury received in the highlands. The aim of the study is to establish the features of animal behavior, homeostatic blood parameters and functional morphology of the cerebellum in TBI in the highlands. The work was performed on 46 white male mongrel rats. The low-mountain series of experiments was modeled at an altitude of 760 m above sea level (Kyrgyzstan, Bishkek), the high-mountain series — at the Tuya-Ashu pass — 3200 m above sea level (Kyrgyzstan). The Weight Drop Method shock model was used to reproduce a traumatic brain injury. The ethology of animals was evaluated in the Open Field test. The lactic acid level was determined in the AQUA LAB (Bishkek). The microcirculation of the cerebellum was examined under the Olympus B×40 microscope (Japan). Statistical data processing was carried out in the SPSS 16.0 program. The visit to the outer squares of the field during TBI decreases (P<0.001) regardless of the height of the experiments, the number of racks in the highlands decreases by 60% (P < 0.001), the number of peeks into minks — by 76 % (P<0.01). The number of acts of defecation after TBI increases. The biochemical parameters of blood in TBI are characterized by an increase in the deficit of buffer bases to −3.8 mmol/l, a drop in the rate of oxygen consumption to 2.5 ml/min, an increase in the ratio between the rate of oxygen transport by arterial blood and the rate of its consumption to 4.8 rel. unit, and the concentration of lactic acid in the blood is up to 5 mmol/l. The microcirculatory bed of the cerebellum in TBI in the highlands is characterized by increased tortuosity, the appearance of swellings and interceptions along the course of blood vessels, activation of anastomoses, increased vascular porosity, hypercapillarization with erythrocyte sludge, parietal standing of leukocytes, the formation of blood clots in all parts of the vascular bed. There is vasogenic swelling of the cerebellum with the phenomena of dislocation of layers.


1982 ◽  
Vol 63 (6) ◽  
pp. 9-11
Author(s):  
A. L. Kirillov

Examined 87 patients with craniostenosis at the age from 3 to 14 years, who had suffered a moderate craniocerebral injury. It was found that in the stage of compensation, a relatively mild traumatic brain injury leads to mild brain contusion. Treatment of patients in this category should be conservative, but longer than in patients without concomitant craniostenosis. In the decompensated stage of craniostenosis, a similar injury causes the development of moderate brain contusion. With severe cerebral edema, flap craniotomy is indicated, since conventional dehydration therapy is ineffective.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
David Tweedie ◽  
Hanuma Kumar Karnati ◽  
Roger Mullins ◽  
Chaim G Pick ◽  
Barry J Hoffer ◽  
...  

Traumatic brain injury (TBI) is a serious global health problem, many individuals live with TBI-related neurological dysfunction. A lack of biomarkers of TBI has impeded medication development. To identify new potential biomarkers, we time-dependently evaluated mouse brain tissue and neuronally derived plasma extracellular vesicle proteins in a mild model of TBI with parallels to concussive head injury. Mice (CD-1, 30–40 g) received a sham procedure or 30 g weight-drop and were euthanized 8, 24, 48, 72, 96 hr, 7, 14 and 30 days later. We quantified ipsilateral cortical proteins, many of which differed from sham by 8 hours post-mTBI, particularly GAS-1 and VEGF-B were increased while CXCL16 reduced, 23 proteins changed in 4 or more of the time points. Gene ontology pathways mapped from altered proteins over time related to pathological and physiological processes. Validation of proteins identified in this study may provide utility as treatment response biomarkers.


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