Sveredyuk Y. Pathogenetic features of electrolyte-steroid cardiomyopathy development and their correction

The thesis provides theoretical generalization and new solution for the current scientific task of finding mechanisms of electrolyte-steroid cardiomyopathy development, due to glucocorticoid dexamethasone action and cardioprotective effects by means of L-carnitine, the specific features of vegetative cardiac control, the sensitivity of myocardial cholinergic receptors, the degree of metabolic and structural impairment in the myocardium, and sexual differences. As a result of the complexis researches, it was revealed pathogenetic lawfulness of electrolyte-steroid cardiomyopathy development in dependence on disorders of neuro-mediator processes, oxidative and nitrooxidative stress, water-electrolytic balance and sexual differences. It was established features of vegetative heart regulation disordes, methabolic and structural disturbances in the heart. It was proved that development of cardiomyopathy in the both sex is acompained by disorders of myocardial electric stability, strain of regulatori systems as display stress reaction with dominance in the mails (p < 0,05). The applay of L-carnitine conduced to normalization of the variation range cardiointervalometry indecies to intact level, mainly in the femails. It was proved that long-term use of dexamethasone (14 days) resulted to weakening of the heart cholinergic regulation as well as in the femails and in the mails for reaction to exogenous and endogenous acetylcholine, especially in condition increased NaCl level in drinking water. Long-term use of dexamethasone with increased content NaCl level in drinking water causes an excessive tone of the sympathetic nervous system, and the use of L-carnitine restores the level in the intact animals, also inhibits cholinesterase activity. It was found that the drug prevents an increase in pure heart weight in the simulated pathology,and the suppression of the antioxidant system and the accumulation of diene, triene conjugates and TBA-active products in the ventricular myocardium in the both sex rats, and increase of nitrite level in serum, ventricles and atria. It was established that dexamethasone causes in the left ventricle structural disfibration, perivascular and stromal edema, perivascular and lymphocytic infiltration (more expressed in the mails than in the femails), which enhanced for salt load, L-carnitine decreased displays of destructive prosses in the myocardium.