NITRITE-ANIONS CONTENT CHANGES IN THE VENTRICLES AND ATRIA MYOCARDIUM OF RATS UNDER CONDITIONS WITH DEVELOPMENT OF ELECTROLYTE-STEROID CARDIOMYOPATHY
Keywords:heart, NO2, dexamethasone, salt, L-carnitine
Introduction. Arterial hypertension and metabolic disorders are often the result of long-term steroid treatment. Eating a diet with high NaCl level can significantly increase this risk. A serious complication due to these disorders is often the development of cardiomyopathy. One of the preventive measures in this case is the nitric monooxide system. L-carnitine, which is an antioxidant, has the ability to influence energy metabolism, apoptosis processes, DNA transcription and it can be a promising means of correcting disturbances in the nitric monooxide system.
The aim of the study – to learn the content of NO2- in the heart of rats under prolonged exposure to dexamethasone, an increased content of NaCl (4 %) in drinking water and under correction with L-carnitine.
Research Methods. The experiment was carried out on 96 white nonlinear rats in compliance with the bioethics standards. The content of nitrite anion was determined in homogenates of the atria and ventricles by the Gris method. Steroid cardiomyopathy was modeled by daily dexamethasone administration for 15 days. Half of the animals received a 4 % NaCl solution in tap water for drinking. Correction was performed with L-carnitine given per OS.
Results and Discussion. It was found that long-term use of dexamethasone and high salt content in water lead to a decrease in NO2- levels in the heart ventricles of rats of both sexes (24 %, p<0.05). L-carnitine demonstrates the ability to restore metabolite levels. The difference between the sexes appears in animals with normal NaCl levels in water. With a high level of salt in the water, the negative changes are more intense and the difference between the sexes is no longer so pronounced. In the atria, only a difference in the content of NO2- between the sexes was found (13 % (p<0.05) lower in males than in females at all stages of the study). Dexamethasone or salt does not affect the metabolite in this tissue.
Conclusions. Steroid-electrolyte damage of the heart is accompanied with a decrease in nitrite anion in the ventricular myocardium, L-carnitine effectively neutralizes these changes. In the atrial myocardium, a difference in the content of nitrite anion was found only depending on gender; dexamethasone or high salt content did not affect this indicator.
Goldberg, J.F., Mery, C.M., Griffiths, P.S., Parekh, D.R., Welty, S.E., Bronicki, R.A., et al. (2014). Extracorporeal membrane oxygenation support in severe hypertrophic obstructive cardiomyopathy associated with persistent pulmonary hypertension in an infant of a diabetic mother. Circulation, 130 (21), 1923-1925.
Shibata, K., Yatera, Y., Furuno, Y., Sabanai, K., Morisada, N., Nakata, S., et al. (2010). Spontaneous development of left ventricular hypertrophy and diastolic dysfunction in mice lacking all nitric oxide synthases. Circulation Journal, 74 (12), 2681-2692.
Goodwin, J.E., & Geller, D.S. (2012). Glucocorticoid-induced hypertension. Pediatric Nephrology, 27 (7), 1059-1066.
Jiang, J., Zhang, J., Kang, M., Yang, J. (2019). Transient hypertrophic cardiomyopathy and hypertension associated with hydrocortisone in preterm infant. Medicine, 98 (33), 1–4.
Lee, J., Bae, E.H., Ma, S.K., Kim, S.W. (2016). Altered Nitric Oxide System in Cardiovascular and Renal Diseases. Chonnam Medical Journal, 52 (2), 81-90.
Paech, C., Wolf, N., Thome, U.H., Knüpfer, M. (2014). Hypertrophic intraventricular flow obstruction after very-low-dose dexamethasone (Minidex) in preterm infants: case presentation and review of the literature. Journal of Perinatology, 34 (3), 244-246.
Guimarães, F.D.S., Wilson, Max Almeida Monteiro De Moraes, Bozi, L.H.M., Souza, P.R., Antonio, E.L., Bocalini, D.S., et al. (2016). Dexamethasone-induced cardiac deterioration is associated with both calcium handling abnormalities and calcineurin signaling pathway activation. Molecular and Cellular Biochemistry, 424 (1-2), 87-98.
Ito, D., Ito, O., Mori, N., Cao, P., Suda, C., Muroya, Y., et al. (2013). Exercise training upregulates nitric oxide synthases in the kidney of rats with chronic heart failure. Clinical and Experimental Pharmacology and Physiology, 40 (9), 617-625.
Bae, E.H., Ma, S.K., Lee, J., Kim, S.W. (2011). Altered regulation of renal nitric oxide and atrial natriuretic peptide systems in angiotensin II-induced hypertension. Regulatory Peptides, 170 (1-3), 31-37.
Bongartz, L.G., Braam, B., Verhaar, M.C., Cramer, M.J., Goldschmeding, R., Gaillard, C.A., et al. (2010). Transient nitric oxide reduction induces permanent cardiac systolic dysfunction and worsens kidney damage in rats with chronic kidney disease. A.merican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 298 (3), 15-23.
Maneesai, P., Bunbupha, S., Potue, P., Berkban, T., Kukongviriyapan, U., Kukongviriyapan, V., et al. (2018). Hesperidin prevents nitric oxide deficiency-induced cardiovascular remodeling in rats via suppressing TGF-β1 and MMPs protein expression. Nutrients, 10 (10), 1549.
Al-Eisa, R.A., Al-Salmi, F.A., Hamza, R.Z., El-Shenawy, N.S. (2018). Role of L-carnitine in protection against the cardiac oxidative stress induced by aspartame in Wistar albino rats. Plos One, 13 (11), 1-12.
How to Cite
Copyright (c) 2021 Medical and Clinical Chemistry
This work is licensed under a Creative Commons Attribution 4.0 International License.