DYNAMICS OF PATHOMORPHOLOGICAL CHANGES OF THE MYOCARDIUM IN CHRONIC EXPERIMENTAL ENDOTOXICOSIS

D. Koval, A.S. Kolosovych, О.О. Levenets, О.І. Hladiy, A. Mykolenko
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Abstract

Relevance. Modeling the conditions of endotoxicosis by introducing bacterial lipopolysaccharide against the background of toxic liver damage is due to the fact that under such conditions the situation that accompanies almost every chronic pathology, including cardiovascular, is reproduced. The release of substances that play a role in the formation of endogenous intoxication causes heart damage in the absence of cardiac pathology, and in its presence worsens the course and prognosis. However, it should be found out whether these changes are the result of only toxic damage to cardiomyocytes or have another morphological basis and what their dynamics are. Objective: to characterize the morphological changes of the myocardium in experimental chronic endotoxicosis. Materials and methods. The research was carried out by modeling endotoxicosis  in 18 laboratory animals for 90 days by daily intragastric injection of tetrachloromethane at the rate of 3-5 ml/kg of body weight and every 6th day by intraperitoneally adding bacterial lipopolysaccharide at a dose of 0.2 mg/kg of body weight. Animals were removed from the experiment by decapitation at 30, 60, and 90 days. Animals were removed from the experiment by decapitation after anesthesia with intraperitoneal administration of sodium thiopental at a dose of 50 mg/kg. The control group consisted of 6 intact animals. For histological examination, myocardial tissue was condensed in paraffin, and deparaffinized sections were stained with hematoxylin and eosin, examined for the detection of neutral glycosaminoglycans and acidic mucopolysaccharides, stained with Alcian blue and PAS-reaction according to standard methods, and examined under a Nikon Eclipse Ci-E light microscope. Results. During researching the myocardium at the light-optical level of experimental animals, after 30 days of chronic endogenous intoxication caused by injection of tetrachloromethane and bacterial LPS, it undergoes changes, first of all, it concerned cardiomyocytes: we observe thinned cells around the vessels and unchanged ones at a distance from the vessels. In some of them, hyperchromia of the nuclei and phenomena of contractile damage and fiber fragmentation were noted. Manifestations from the CMC increased during the next period of the experiment: after 60 days, expressed wave-like deformation of fibers with atrophic changes in muscle cells was detected in the myocardium. Hemodynamic changes were characterized by hyperemia, the number of perivascular hemorrhages increased. On the 90th day of the experiment, in addition to inflammatory manifestations and dystrophic-necrotic changes, cardiomyocyte atrophy in combination with expressed interstitial edema was detected in the myocardial tissue of animals. In the stroma, in addition to small foci of perivascular cardiosclerosis, foci of adipocyte growth were determined. Cardiomyocyte defibrillation and hemorrhages were observed in some areas Conclusion. The intensity of structural changes in cardiomyocytes and hemodynamic disorders in chronic endotoxicosis depends on the duration of intoxication and the character of structural changes. The interstitium of the myocardium of rats under experimental endotoxicosis conditions is dystrophic-sclerotic and is manifested by a different combination of edematous and sclerotic manifestations at different stages of exposure to toxicants.
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慢性实验性内毒素血症心肌病理形态学变化的动力学研究
关联在毒性肝损伤的背景下,通过引入细菌脂多糖来模拟内毒素血症的条件,是因为在这种条件下,几乎所有慢性病理(包括心血管)都会出现这种情况。在没有心脏病理学的情况下,在内源性中毒形成中起作用的物质的释放会导致心脏损伤,并且在其存在的情况下会恶化病程和预后。然而,应该弄清楚这些变化是仅仅是心肌细胞毒性损伤的结果,还是有另一个形态学基础,以及它们的动力学是什么。目的:观察实验性慢性内毒素血症心肌的形态学变化。材料和方法。本研究通过在18只实验动物中模拟内毒素血症进行,为期90天,每天以3-5ml/kg体重的速率胃内注射四氯化碳,每6天腹膜内添加0.2mg/kg体重的细菌脂多糖。在第30、60和90天通过斩首将动物从实验中移除。麻醉后用50mg/kg剂量的硫喷妥钠腹膜内给药,通过斩首将动物从实验中取出。对照组由6只完整的动物组成。对于组织学检查,将心肌组织在石蜡中浓缩,并用苏木精和伊红对脱蜡切片进行染色,检测中性糖胺聚糖和酸性粘多糖,根据标准方法用阿尔西安蓝和PAS反应进行染色,并在Nikon Eclipse Ci-E光镜下进行检查。后果在实验动物的光学水平上研究心肌时,在注射四氯化碳和细菌LPS引起的慢性内源性中毒30天后,它发生了变化,首先是心肌细胞:我们观察到血管周围的细胞变薄,而在离血管一定距离处的细胞不变。在其中一些中,注意到细胞核的超染色以及收缩损伤和纤维断裂的现象。CMC的表现在实验的下一阶段增加:60天后,在心肌中检测到纤维的波浪状变形和肌肉细胞的萎缩性变化。血液动力学变化以充血为特征,血管周围出血次数增加。在实验的第90天,除了炎症表现和营养不良坏死变化外,在动物的心肌组织中还检测到心肌细胞萎缩并伴有表达的间质水肿。在基质中,除了血管周围心脏硬化的小病灶外,还确定了脂肪细胞生长的病灶。部分区域出现心肌细胞除颤及出血。慢性内毒素血症心肌细胞结构变化的强度和血液动力学障碍取决于中毒的持续时间和结构变化的特征。在实验性内毒素血症条件下,大鼠心肌的间质是营养不良硬化的,并且在暴露于毒物的不同阶段表现为水肿和硬化的不同组合。
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