REMODELING OF RAT’S HEART IN CONDITIONS OF METABOLIC CARDIOMYOPATHY DEVELOPMENT AND POSSIBILITIES OF ITS CORRECTION
DOI:
https://doi.org/10.11603/1811-2471.2020.v.i2.11331Keywords:
cardiomyopathy, dexamethasone, L-carnitine, morphometryAbstract
Anti-inflammatory and immunosuppressive therapy often includes using glucocorticosteroids, but after long-term their use for treatment of chronic diseases especially often arise unfavorable and secondary complications. One of them is metabolic cardiomyopathy. On the other hand, aminoacid L-carnitine has important property in particular it promotes to transport lipids inside mitochondria. In the experimental model of steroid cardiomyopathy was demonstrated that L-carnitine preventes development of heart massometric remodeling reducing catabolic action of the dexamethasone thus normalizes total weight body and in particular absolute weight of the left and the right ventricle of the heart, damaged by dexamethasone.
The aim – to determinate the possibility of prevention of structural dystrophic changes development in the rat’s heart of different sex owing to long-term use corticosteroids.
Material and Methods. Experiments were performed on 48 adult white rats of different sex, which were divided into 4 groups. The total weight of animal, absolute weight of left and right ventricles of heart were measured (morphometry) in the experiment.
Conclusions. L-carnitine (in dose 200 mg/kg of animal weight per os) has the ability to significantly reduce the catabolic effects of dexamethasone and thus normalization of body weight and absolute weight of the left and right ventricles of heart. That L-carnitine (in dose 350 µg/kg of animal body weight per os) is able to prevent massometric remodeling of the heart in modelled cardiomyopathy. The studing of structural-degenerative changes on the base determination of the ratio masses/volumes of cardiomyocytes to connective tissue it is perspective.
References
Alan, I. S., & Alan, B. (2018). Side effects of glucocorticoids. Pharmacokinetics and Adverse Effects of Drugs – Mechanisms and Risks Factors, 93-115. DOI:10.5772/intechopen.72019. DOI: https://doi.org/10.5772/intechopen.72019
Goodwin, J.E., Zhang, X., Rotllan, N., Feng, Y., Zhou, H., Fernández-Hernando, C., Sessa, W.C. (2015). Endothelial glucocorticoid receptor suppresses atherogenesis – brief report. Arteriosclerosis, Thrombosis, and Vascular Biology, 35 (4), 779-782. DOI:10.1161/atvbaha.114.304525. DOI: https://doi.org/10.1161/ATVBAHA.114.304525
Gupta, Y., & Gupta, A. (2013). Glucocorticoid-induced myopathy: Pathophysiology, diagnosis, and treatment. Indian Journal of Endocrinology and Metabolism, 17 (5), 913-925. DOI:10.4103/2230-8210.117215. DOI: https://doi.org/10.4103/2230-8210.117215
Liu, Zhang, Knight, & Goodwin (2019). The glucocorticoid receptor in cardiovascular health and disease. Cells, 8 (10), 1227-1149. DOI:10.3390/cells8101227. DOI: https://doi.org/10.3390/cells8101227
Nishida, K., & Otsu, K. (2017). Inflammation and metabolic cardiomyopathy. Cardiovascular Research, 113 (4), 389-398. DOI:10.1093/cvr/cvx012 DOI: https://doi.org/10.1093/cvr/cvx012
Ren, R., Oakley, R.H., Cruz-Topete, D., & Cidlowski, J.A. (2012). Dual role for glucocorticoids in cardiomyocyte hypertrophy and apoptosis. Endocrinology, 153 (11), 5346-5360. DOI:10.1210/en.2012-1563 DOI: https://doi.org/10.1210/en.2012-1563
Qi, D., Pulinilkunnil, T., An, D., Ghosh, S., Abrahani, A., Pospisilik, J.A., & Rodrigues, B. (2004). Single-dose dexamethasone induces whole-body insulin resistance and alters both cardiac fatty acid and carbohydrate metabolism. Diabetes, 53 (7), 1790-1797. DOI:10.2337/diabetes.53.7.1790 DOI: https://doi.org/10.2337/diabetes.53.7.1790
European convention for the protection of vertebrate animals used for experimental and other scientific purposes. (1986). Strasbourg: Council of Europe.
Kopple, J.D. (2002). L-carnitine ameliorates gentamicin-induced renal injury in rats. Nephrology Dialysis Transplantation,17 (12), 2122-2131. DOI: https://doi.org/10.1093/ndt/17.12.2122
Roy, S.G., De, P., Mukherjee, D., Chander, V., Konar, A., Bandyopadhyay, D., & Bandyopadhyay, A. (2009). Excess of glucocorticoid induces cardiac dysfunction via activating angiotensin II pathway. Cellular Physiology and Biochemistry, 24 (1-2), 1-10. DOI: https://doi.org/10.1159/000227803
Avtandilov, G.G. (2002). Osnovy kolichestvennoy patologicheskoy anatomii [Bases of quantitative pathological anatomy]. Moscow: Meditsina [in Russian].
