PATHOGENETIC VALUE OF CARDIOPATHY MARKERS IN HEART LESION OF ANIMALS WITH SYSTEMIC LUPUS ERYTHEMATOSUS EXPERIMENTAL MODEL
Summary. Background. Heart pathology in systemic lupus erythematosus (SLE) refers to the most common manifestations of the disease and largely determines its prognosis. The pathogenetic constructions of myocardium, endocardium and coronary vessel lesions remain insufficiently studied. The evaluation of lupus cardiopathy separate pathogenetic aspects is carried out on native models in some linear mice. The aim of the research: to study the blood cardiopathy markers in experimental animals (rats) with SLE model and to evaluate their pathogenetic significance in cardiomyocytes, myocardium, endocardium, valves and cardiac vessels damage. Material and methods. The SLE modelling was performed in 53 white non-breeding rats (34 females and 19 males) using full Freund’s adjuvant, splenic deoxyribonucleic acid of cattle, cyclophosphamide, azid and sodium deoxyribonucleate. Cadmium sulfate, lithium oxybutyrate and ammonium molybdate were added for feeding animals. The levels of endothelin-1, thromboxane A2, prostacyclin, interleukin-6, tumor necrotic factor a, homocysteine, apelin, atrial and brain natriuretic peptide (BNP), N-terminal prohormone of the latter (NT-BNP). Results. In the animals with SLE model, there are changes in blood markers of experimental lupus cardiopathy, reflecting the state of the vessel endothelial function, the proinflammatory cytokine chain and natriuretic peptides, which are manifested by significant increase by 10% of endothelin-1 concentration, respectively, by 54% of interleukin-6 content and the ratio of this cytokine with tumor necrosis factor-alfa, by 73% of BNP level, which was found in 36; 66; 62 and 13% of the examined rats number. Conclusions. The studied cardiopathic markers determine the coronary vessel damage, while the indices of apelin adipocytokine and natriuretic hormones of type A and B are involved in the development of cardiomyocyte (hypertrophy, dystrophy, necrosis) and myocardial stroma changes (edema, cellular infiltration, sclerosis), and the heart structure lesion severity depends on the values of BNP and NT-BNP.
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