模拟高同型半胱氨酸血症、甲亢、甲减及其联合作用下动物心肌超微结构的变化

V. Nechiporuk, L. О. Pentyuk, O. Kovalchuk, O. I. Mazur, M. Korda
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摘要

甲状腺激素通过基因组和非基因组效应对心脏功能有显著影响。甲状腺激素缺乏或过量导致心功能和心血管血流动力学的调节发生深刻变化。心脏是甲状腺激素作用的主要靶器官,在甲状腺功能低下或甲状腺功能亢进的患者中,心脏的工作有明显的变化。本研究的目的是在甲状腺功能亢进和功能减退的背景下,建立实验性高同型半胱氨酸血症(HHCy)心肌成分的超微结构变化。以硫代内酯形式给予动物外源性HCy,剂量为100 mg/kg体重,每天1次,持续28天。甲状腺机能亢进是通过每天给药200 μg/kg的l -甲状腺素来模拟的,持续21天;甲状腺机能减退是通过每天给药10 mg/kg的噻马唑来模拟的,持续21天。各组动物在服用HCy的同时给予l -甲状腺素和噻马唑。高水平的HCy对心肌血管壁有不利影响。毛细血管管腔充盈,充满红细胞。内皮细胞改变,心肌细胞核变形。在甲亢实验动物中,血管壁超微结构变化增加(毛细血管壁水肿,线粒体嵴受损)。在甲状腺机能亢进和HHCy模型的动物中,内皮细胞发生了更显著的变化,大部分线粒体被破坏。心肌细胞的变化更为明显。甲状腺功能减退动物心肌电镜检查,血管壁超微结构明显退行性改变,线粒体肥大。与其他各组动物相比,甲状腺功能减退和HHCy的共同影响对心肌细胞和毛细血管的超微结构造成了最严重的干扰。细胞间接触完整性受损,肌细胞嵴和外膜大部分线粒体被破坏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ultrastructural changes in the myocardium of animals under conditions of simulated hyperhomocysteinemia, hyper- and hypothyroidism and their combination
Thyroid hormones have a significant impact on heart function through both genomic and non-genomic effects. Deficiency or excess of thyroid hormones leads to profound changes in the regulation of cardiac function and cardiovascular hemodynamics. The heart is the main target organ for the action of thyroid hormones and in patients with hypo- or hyperthyroidism there are marked changes in the work of the heart. The aim of the work was to establish ultrastructural changes in myocardial components in experimental hyperhomocysteinemia (HHCy) against the background of hyper- and hypothyroidism. Thiolactone HHCy was modelized by administering to animals an exogenous HCy in the form of thiolactone at a dose of 100 mg/kg body weight once a day for 28 days. Hyperthyroidism was modelized by daily administration of L-thyroxine at a dose of 200 μg/kg for the 21 days, hypothyroidism – daily administration of thiamazole at a dose of 10 mg/kg for the 21 days. Individual groups of animals were administered L-thyroxine and thiamazole in parallel with HCy. High levels of HCy adversely affected the walls of myocardial blood vessels. The lumens of hemocapillaries were plethoric, filled with erythrocytes. Changes in endotheliocytes were revealed, and cardiomyocytes contained deformed nuclei. In laboratory animals with hyperthyroidism, an increase in ultrastructural changes in the walls of blood vessels (edema of the walls of hemocapillaries, damaged cristae in mitochondria) were established. In animals that were modeled for hyperthyroidism and HHCy, more significant changes in endotheliocytes were revealed, most of the mitochondria were destroyed. More pronounced alterative changes were revealed in cardiomyocytes. An electron microscopic examination of the myocardium of animals with hypothyroidism showed significant degenerative changes in the ultrastructure of the walls of blood vessels, and hypertrophied mitochondria were also found. The combined influence of hypothyroidism and HHCy caused the most profound disturbances in the ultrastructure of cardiomyocytes and hemocapillaries in comparison with other groups of animals. The integrity of intercellular contacts was impaired, most of the mitochondria of myocytes had destroyed cristae and the outer membrane.
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