[PATHOLOGICAL CHANGES DEVELOPMENT IN THE HEART WITH UNDERLYING CONVULSIVE SYNDROME MODEL OF VARIOUS ETIOLOGIES.]

N Kolesova, L Natrus, T Bryuzhina, V Lytvynenko, N Suhareva, S Chukhrai
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Abstract

The basic mechanisms of myocardial damage were determined experimentally in case of electroconvulsive (n = 30) and corazole (n = 20) induced seizures in Wistar rats by histochemical, pathological, electron microscopy and biochemical methods. It has been founded that pathological changes in the myocardium underlying with electroconvulsive and corazole induced seizures have unidirectional origin; nevertheless electrocohvulsive model has more intensity. It has been shown that structural base of myocardial pathology development results in parallel changes of microvessels and contractile myocardium with the main focus on development of contractile changes of cardiomyocytes and intramuscular capillaries spasm, which causes blood flow impairment and reducing supply of oxygen to the working cells. Structural changes in the myocardium develop due to energy shifts which have been elucidated by confirmed decrease SDG in cardiac activity (control 2,65±0,03 act. Units; electroconvulsive model 2,15±0,02 act. Units; and corazole model 2,25±0,02 act. Units), and increased - LDH (control 2,20±0,01 act. Units. electroconvulsive model 2,55±0,01 act. Units; corazole model 2,45±0,01 act. Units.) histochemically, showing evidence of hypoxia progression in the myocardium tissue. It has been also shown processes of increasing degradation as well as reducing synthesis of ATP biochemically(43% electroconvulsive model and 41% corazole model). All this results indicate the presence of hypoenergetics in case of elec- troconvulsive and corazole experimental models of seizures. The received results of complex researches allow considering that adequate and rational treatment and prevention of seizures (large and small epilepsy) requires anticonvulsants choose as well as drug correction of the most affected parts of energy metabolism via afitihypoxants and antioxidants administration. Key words: electroconvulsive and carozole convulsive syn- dromes; heart; metabolism; structure; pathogenesis.

[心脏病变发展伴各种病因的潜在惊厥综合征模型]
采用组织化学、病理、电镜和生化等方法,对电惊厥(n = 30)和科拉唑(n = 20)诱发的Wistar大鼠心肌损伤的基本机制进行了实验研究。已经发现,电惊厥和科拉唑诱发的癫痫发作所引起的心肌病理改变具有单向性;而电痉挛模型的强度更大。研究表明,心肌病理发展的结构基础导致微血管和收缩性心肌的平行变化,主要集中在心肌细胞收缩性变化和肌内毛细血管痉挛的发展,导致血流障碍和工作细胞供氧减少。心肌的结构变化是由于能量转移而发生的,这一变化已被证实为心脏活动SDG的降低(对照2,65±0,03)。单位;电惊厥型2,15±0.02 act。单位;而科诺唑型2,25±0.02 act。单位),并增加- LDH(对照2,20±0.01 act)。单位。电惊厥模型2,55±0.01 act。单位;科拉唑模型2,45±0.01 act。单位)组织化学,显示心肌组织缺氧进展的证据。它还显示了增加降解和减少ATP合成的生化过程(43%电惊厥模型和41%科拉唑模型)。所有这些结果表明,在电惊厥和科拉唑发作的实验模型中存在能量低下。复杂的研究结果表明,充分和合理的治疗和预防癫痫发作(大癫痫和小癫痫)需要抗惊厥药物的选择,以及通过服用抗氧剂和抗氧化剂对能量代谢受影响最大的部分进行药物纠正。关键词:电惊厥和卡罗唑惊厥综合征;心;新陈代谢;结构;发病机理。
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