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Mildronat Meldonium is a precursor to carnitine, a structural analogue of gamma-butyrobetaine (GBB), in which one carbon atom is replaced by a nitrogen atom. Its effect on the body can be explained in two ways.

1. Effect on carnitine biosynthesis.

Meldonium, by reversibly inhibiting gamma-butyrobetaine hydroxylase, reduces the biosynthesis of carnitine and therefore prevents the transport of long-chain fatty acids through cell membranes, thus preventing the accumulation of a strong detergent in cells – activated forms of unoxidized fatty acids. Thus, damage to cell membranes is prevented.

When the concentration of carnitine decreases under ischemic conditions, beta-oxidation of fatty acids is delayed and oxygen consumption in cells is optimized, glucose oxidation is stimulated and the transport of adenosine triphosphate (ATP) from the sites of its biosynthesis (mitochondria) to the sites of consumption (cytosol) is resumed. Essentially, cells are supplied with nutrients and oxygen, and the use of these substances is optimized.

In turn, with an increase in the biosynthesis of the carnitine precursor, i.e. GBB, NO synthetase is activated, resulting in improved rheological properties of the blood and a decrease in peripheral vascular resistance.

With a decrease in the concentration of meldonium, the biosynthesis of carnitine increases again and the amount of fatty acids in the cells gradually increases.

It is believed that the basis for the effectiveness of meldonium is an increase in tolerance to cellular load (with a change in the amount of fatty acids).

2. The function of a mediator in a hypothetical GBB-ergic system. Mildronat

It has been hypothesized that the body has a system for the transfer of neuronal signals – the GBB-ergic system, which ensures the transfer of nerve impulses between cells. The mediator of this system is the last precursor of carnitine – GBB ester. As a result of the action of GBB esterase, the mediator gives the cell an electron, thus transferring an electrical impulse and turns into GBB. Next, the hydrolyzed form of GBB is actively transported to the liver, kidneys and ovaries, where it is converted into carnitine. In somatic cells, in response to irritation, new GBB molecules are again synthesized, ensuring the propagation of the signal.

As the concentration of carnitine decreases, GBB synthesis is stimulated, resulting in an increase in the concentration of GBB ester. Mildronat

Meldonium, as stated earlier, is a structural analogue of GBB and can act as a “mediator”. In contrast, GBB hydroxylase does not “recognize” meldonium, so the carnitine concentration does not increase, but decreases. Thus, meldonium, both by replacing the “mediator” and by promoting an increase in the concentration of GBB, leads to the development of a response in the body. As a result, overall metabolic activity also increases in other systems, such as the central nervous system (CNS).

Effect on the cardiovascular system.

Animal studies have established that meldonium has a positive effect on myocardial contractile activity, it has a myocardioprotective effect (including against catecholamines and alcohol), it can prevent heart rhythm disturbances and reduce the area of myocardial infarction.

Coronary heart disease (stable angina pectoris).

Analysis of clinical data on the course use of meldonium in the treatment of stable angina pectoris showed that the drug reduces the frequency and intensity of angina attacks, as well as the amount of glyceryl trinitrate that is used. The drug exhibits a pronounced antiarrhythmic effect in patients with coronary heart disease (CHD) and ventricular extrasystoles, less effect is observed in patients with supraventricular extrasystoles.


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