林丹和重铬酸钠对心肌血管壁结构特征及血浆同型半胱氨酸含量的影响

S. Rakhmanov, P. A. Elyasin, A. Balmagambetova, A.B. Zhanabaeva, N.A. Zhumabaj
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摘要

的目标。测定在实验条件下暴露于重铬酸钠和林丹时,心室心肌血管壁指标和血液中同型半胱氨酸水平。研究方法。该实验是在雄性小鼠身上进行的;采用组织学方法,对获得的数据进行形态计量学分析,生化血液分析,并对研究数据进行统计处理。结果。实验第1个月暴露于重铬酸钠时,左心室前壁心肌动脉较对照组增厚3.8 px,实验第2个月该指标与对照组接近。两组比较,未见明显变化。左心室后壁心肌动脉的变化与前壁动脉相似。同型半胱氨酸在第1个月暴露于重铬酸钠下的含量较高,在实验的第2个月与第1个月相比略有下降。林丹治疗组在实验第1个月和第2个月的数据与对照组接近。结论。长期暴露于重铬酸钠和林丹会导致壁内动脉壁增厚,同时伴随着血液中内皮功能障碍标志物-同型半胱氨酸水平的增加,同时进一步增加对心肌动脉壁的损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
STRUCTURAL FEATURES OF THE WALL OF MYOCARDIAL INTRAMURAL VESSELS AND THE CONTENT OF HOMOCYSTEIN IN THE BLOOD PLASMA UNDER THE LINDANE AND SODIUM DICHROMATE EXPOSURE
Aim. Determine indicators of the vascular wall of the ventricular myocardium and the level of homocysteine in the blood when exposed to sodium dichromate and lindane under experimental conditions. Methods of the Research. The experiment was carried out on male mice; the histological method, morphometry of the obtained data, biochemichal blood analysis, and the statistical processing of the research data were used. Results. When exposed to sodium dichromate in the 1st month of the experiment, the myocardial arteries of the anterior wall of the left ventricle were thickened by 3.8 px compared with the control, in the 2nd month of the experiment this indicator was close to those of the control group. When compared between the two experimental groups, no clear changes were found. The revealed changes in the myocardial artery of the posterior wall of the left ventricle are similar to those of the anterior wall artery. The content of homocysteine under the exposure to sodium dichromate in the 1st month is higher, in the 2nd month of the experiment it is slightly reduced compared to the 1st month. The data obtained in the lindane treatment group both in the 1st and 2nd months of the experiment were close to those of the control group. Conclusion. Chronic exposure to sodium dichromate and lindane causes thickening of the walls of the intramural arteries, which was accompanied by an increase in the level of the endothelial dysfunction marker — homocysteine in the blood, while increasing further damage to the walls of the arteries in the myocardium.
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