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

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.