AB0176 Morphological heart changes in animals with experimental systemic lupus erythematosus

Autor: Y. Yehudina, Tetyana Bevzenko, O. Syniachenko
Rok vydání: 2018
Předmět:
Zdroj: SLE, Sjögren’s and APS – etiology, pathogenesis and animal models.
Popis: Background Heart pathology in systemic lupus erythematosus (SLE) refers to the most common manifestations of the disease and largely determines its prognosis.. 1 2 The pathogenetic constructions of myocardium, endocardium and coronary vessel lesions remain insufficiently studied.. 3 4 Histological evaluation of separate cardiac structures is performed on native models of SLE in linear mice. Objectives to study in the experiment on animals (rats) with SLE model the degree of cardiomyocytes, myocardium, endocardium, valves and cardiac vessel damage, comparing the results with thymus and spleen tissues histological data. 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. Histological heart specimen were stained with hematoxylin and eosin, altsyon blue (pH=2.6), van Gieson. PAS-reaction was applied. Results Experimental SLE is accompanied by the development of cardiopathy in all animals with cardiomyocytes hypertrophy, dystrophy and necrosis, morphological signs of coronary vessel, myocardial stroma, endocardium and heart valves sclerosis, proliferation of vascular endothelium, which has dispersion and direct correlation relationships with the degree of lymphoma-macrophage infiltration, interstitial tissue, perivascular and valvular histiocytic cell infiltration, and the vessels endothelium damage nature is closely linked to the presence of mast cells in myocardial stroma, it is defined by endocardium necrosis and valves collagenolysis, decrease in spleen lymphoid tissue, and also in the brain layer cells and Gassal cells in the thymus. Conclusions In the case of experimental lupus cardiopathy, there is determine heart structures lesion, what is more, the immune disorders are involved in their pathogenetic constructions, as indicated by the damage of the immunocompetent organs’ (thymus and spleen) corresponding structures. References [1] Falasinnu T, Chaichian Y, Simard JF. Impact of sex on systemic lupus erythematosus-related causes of premature mortality in the United States. J. Womens Health2017;26(11):1214–1221. [2] Hasham MG, Baxan N, Stuckey DJ, et al. Systemic autoimmunity induced by the TLR7/8 agonist Resiquimod causes myocarditis and dilated cardiomyopathy in a new mouse model of autoimmune heart disease. Dis. Model Mech2017;10(3):259–270. [3] Mavrogeni S, Koutsogeorgopoulou L, Markousis-Mavroge- nis G, et al. Cardiovascular magnetic resonance detects silent heart disease missed by echocardiography in systemic lupus erythematosus. Lupus2013;1(1):961203317731533. [4] Myung G, Forbess LJ, Ishimori ML, et al. Prevalence of resting-ECG abnormalities in systemic lupus erythematosus: a single- center experience. Clin. Rheumatol2017;36(6):1311–1316. Disclosure of Interest None declared
Databáze: OpenAIRE