METABOLIC EFFECTS OF β-BLOCKERS METOPROLOL, AMP AND ADENOSINE IN SYMPATHETIC HYPERACTIVATION

Abstract

Relevance: Currently, in cardiology, in order to develop adequate methods of treatment of cardiovascular diseases, it is very important to establish the mechanisms of violation of adaptive processes observed in sympathetic hyperactivation. As many studies show, myocardial ischemia is accompanied by a significant increase in the content of adrenaline in the heart. In the area of myocardial ischemia, its concentration increases by more than 1.5-2 times compared with background data; in remote areas of the heart – by 1.4-1.6 times. At the same time, there is a progressive decrease in the content of adrenaline in the adrenal glands. This indicates mainly the adrenal origin of adrenaline in the muscles of the heart [2]. Purpose of the study: To study the effect of purine nucleotide metabolites (AMP and adenosine) and the selective β1- adrenergic blocker metoprolol on sympathetic hyperactivation. Materials and methods. The study was conducted on 160 male albino rats, aged 3–3.5 months, weighing 225 (95% SA: 203–238) grams. The experiment was divided into 3 series. Main research methods: The activity of glutathione reductase (GR) and glutathione peroxidase (GPO) was determined according to the method of S.N. Vlasova and co-authors. Biochemical research methods were used. The amount of protein was determined by the Lowry method. The amount of phosphoric acid was calculated from the calibration graph. The activity of adenosine monophosphate deaminase (AMP deaminase) and adenosine deaminase was determined according to the method of S.O. Tapbergenova. The determination of the amount of MDA was carried out according to the method of Uchiyama M., Mihara M., diene conjugates according to the method of V.B. Gavrilov and co-authors. The results of the study. Like adrenaline, metoprolol increases the total number of white blood cells, lymphocytes, reduces the number of T-suppressors, HCT. In serum, hyperadrenalinemia causes activation of AMPD, AD, 5'H and GPO, increases the level of PC. Due to a slight increase in blood pressure activity in the blood serum, the ratio "B" (ratio of blood pressure / AMPD activity) increases. As previously established, an increase in the "B" coefficient indicates an increase in the functional interaction of T- and B-links of immunity in sympathetic hyperactivation. Metoprolol, an adrenaline-like cardioselective β1 blocker, causes activation of the enzymes AMPD, BP and 5H in the blood serum, increases the level of factor B and PK, but unlike adrenaline, metoprolol reduces the activity of GPO and catalase and reduces the level of MDA. Conclusion. Analysis of the data obtained allows us to conclude that during sympathetic hyperactivation, both β1- adrenergic blockade in the heart and the administration of AMP and adenosine to animals at the indicated dose reduce the process of peroxidation and adequately reduce the activity of antioxidant defense enzymes.