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Instructions for use MILDRONATUM

A drug that improves metabolism. It is a structural analogue of the carnitine precursor gamma-butyrobetaine (GBB), in which one hydrogen atom is replaced by a nitrogen atom.

It is assumed that there are 2 mechanisms of action of Mildronate on the body

1. Effect on carnitine synthesis

As a result of inhibition of the activity of butyrobetaine hydroxylase, Mildronate reduces the biosynthesis of carnitine and inhibits the transport of long-chain fatty acids through the cell membrane, preventing the accumulation in cells of activated derivatives of unoxidized fatty acids - acylcarnitine and acyl coenzyme A, which have pronounced detergent properties. Under ischemic conditions, Mildronate restores the balance between oxygen delivery and consumption in cells, eliminates disturbances in ATP transport, while simultaneously activating an alternative energy source - glycolysis, which occurs without additional oxygen consumption.

With increased load, as a result of intensive energy consumption, a temporary decrease in the content of fatty acids, mainly carnitine, occurs in the cells of a healthy body. It is known that carnitine biosynthesis is regulated by its level in the blood plasma and stress, but does not depend on the concentration of carnitine precursors in the cell. Since Mildronate inhibits the conversion of GBB to carnitine, this leads to a decrease in the level of carnitine in the blood, which in turn activates the process of synthesis of the carnitine precursor - GBB.

When the concentration of Mildronate decreases, the process of carnitine biosynthesis is restored and the concentration of fatty acids in the cell is normalized. Thus, the cells undergo regular training, which contributes to their survival under conditions of increased load, in which the content of fatty acids in them regularly decreases, and when the load decreases, the fatty acid content is quickly restored. Under real overload conditions, cells “trained” with Mildronate survive in conditions where “untrained” cells die.

2. Function of the mediator of the hypothetical GBB-ergic system

It has been hypothesized that in the body there is a previously undescribed system for the transmission of nerve impulses - the GBB-ergic system, which ensures the transmission of nerve impulses to somatic cells. The mediator of this system is the immediate precursor of carnitine, the GBB ester. As a result of the action of esterase, this transmitter gives the cell an electron, thus transferring an electrical impulse, and itself turns into GBB.

GBB synthesis is possible in any somatic cell of the body. Its speed is regulated by the intensity of the stimulus and energy expenditure, which in turn depend on the concentration of carnitine. Therefore, when carnitine concentration decreases, GBB synthesis is stimulated. When the concentration of a mediator (GBB ester) increases in any place in the body, with the participation of the central nervous system, regulatory mechanisms are activated that are “responsible” specifically for it.

Thus, the body has an economical chain of reactions that provides an adequate response to irritation or stress:

it begins with the receipt of a signal from nerve fibers (in the form of an electron), followed by the synthesis of GBB and its ester, which, in turn, transfers the signal to the membranes of somatic cells. Somatic cells, in response to irritation, synthesize new molecules, ensuring the propagation of the signal. After this, the hydrolyzed form of GBB, with the participation of active transport, enters the liver, kidneys and testes, where it is converted into carnitine.

As stated earlier, Mildronate is a structural analogue of GBB, in which one hydrogen atom is replaced by a nitrogen atom. Since Mildronate can be affected by GBB esterase, it may function as a hypothetical "mediator". However, GBB hydroxylase does not act on mildronate and therefore, when it is introduced into the body, the concentration of carnitine does not increase, but decreases. Due to the fact that Mildronate itself acts as a “mediator” of stress and also increases the content of GBB, it contributes to the development of the body’s response. As a result, overall metabolic activity increases in other systems, for example, the central nervous system.

Experimental results

In experiments on anesthetized cats, the effect of mildronate on indicators of the cardiovascular system was studied. It has been established that over a wide range of doses, the drug increases blood flow, systolic and minute volumes, does not have a significant effect or slightly reduces venous pressure. These data indicate a positive effect of Mildronate on myocardial contractile function.

Mildronate has a protective effect against myocardial hypoxia. In experiments on isolated rabbit atria, it was found that after the cessation of hypoxic effects, the drug accelerates the restoration of myocardial contractility to a normal level.

In another series of experiments on anesthetized white rats, it was revealed that the administration of Mildronate before the start of the experiment eliminates the increase in ischemia (ST segment elevation) after ligation of the left coronary artery, reduces the corresponding focus of the infarction and increases the life expectancy of the animals. Upon repeated administration of the drug for 10 days, a pronounced (more than 2-fold compared to the control) reduction in the infarction focus was detected.

Mildronate is more effective than nifedipine in preventing the development of heart rhythm disturbances, including ventricular fibrillation, in rats after ligation of the coronary arteries.

In conditions of “lightened” experimental myocardial infarction (ligation of the left coronary artery for ≤1 hour) in dogs, the drug eliminates ischemic ECG changes.

Mildronate protects the myocardium from the damaging effects of catecholamines and alcohol.

In experiments on rats, it was found that preliminary administration of Mildronate in 50% of animals completely eliminates ECG changes caused by isoproterenol (isadrin) and epinephrine (adrenaline). Histological examination of the myocardium of rats indicates that when epinephrine is used, mildronate protects myocardial cells, prevents the development of irreversible changes in cardiomyocytes and promotes the restoration of normal myocardial structure.

Experimental studies have established that myocardial damage caused by toxic concentrations of ethyl alcohol is, in principle, no different from those caused by ischemia or stress. It can be assumed that this is due to the similarity of the mechanisms of action of factors affecting myocardial tissue. The data that Mildronate reduces myocardial damage caused by ethyl alcohol serves as a justification for the use of the drug for the correction of functional and organic disorders of the body in chronic alcohol intoxication.

It has been experimentally established that Mildronate reduces the stimulating effect of ethyl alcohol by approximately 5 times. Under “free choice” conditions, mildronate reduces the consumption of ethyl alcohol by experimental animals by 80-100%.

In animal experiments, the antihypoxic and cerebral blood flow-improving effects of the drug were observed. It has been established that Mildronate has a positive effect in ischemia of brain tissue. The drug optimizes the distribution of cerebral blood flow in favor of ischemic foci and increases the resistance of neurons to hypoxia. Thus, in experiments on rats, the drug partially or completely eliminated EEG changes after occlusion of the carotid artery. Mildronate has an activating effect on the central nervous system:

motor activity and physical performance increase, stimulation of motor reactions is noted, as well as an anti-stress effect, manifested in stimulation of the sympathetic nervous system, an increase in the content of catecholamines in the brain and adrenal glands, and a protective effect against stress-induced changes in internal organs.

The obtained results of experimental studies indicate the effectiveness of Mildronate and the possibility of its use in cerebrovascular pathology.

Clinical trial results

Analysis of clinical data on the course of treatment of stable angina with Mildronate indicates that under the influence of the drug the frequency and intensity of attacks are reduced, and the amount of nitroglycerin used is also reduced. The drug has a pronounced antiarrhythmic effect in the presence of ischemic heart disease and ventricular extrasystoles and is less effective in supraventricular extrasystoles. Particularly noteworthy is the drug’s ability to reduce oxygen consumption at rest, which is considered an indicator of the effectiveness of antianginal treatment of coronary artery disease. Mildronate has a beneficial effect on atherosclerotic processes in the coronary and other peripheral vessels as a result of reducing the level of total cholesterol in the blood plasma and the atherogenic index.

The role of Mildronate in the treatment of chronic heart failure due to coronary artery disease has been analyzed on the basis of a fairly large number of clinical studies, which indicate that the drug increases exercise tolerance and the amount of work performed by patients suffering from heart failure.

In a separate study from the Latvian and Tomsk Institutes of Cardiology, the effectiveness of Mildronate in moderate heart failure (functional class II according to the NYHA classification) was studied. After treatment with Mildronate, 59-78% of patients with an initial diagnosis of functional class II heart failure were assigned to the functional class I group.

It has been established that Mildronate improves myocardial inotropic function and increases exercise tolerance, improves the quality of life of patients without causing severe side effects. It is noted, however, that Mildronate can cause moderate arterial hypotension, allergic skin reactions, headaches, and a feeling of discomfort in the pit of the stomach. In severe heart failure, Mildronate should be prescribed in combination with traditional drugs used to treat this disease.

A good clinical effect of Mildronate was observed in patients with cardialgia that developed as a result of menopause and alimentary obesity.

In clinical settings, it has been established that treatment with Mildronate reduces the frequency of relapses of alcoholism. Mildronate has been shown to relieve alcohol withdrawal syndrome.

Mildronate is an effective means of complex treatment of acute and chronic cerebrovascular accidents (ischemic stroke, chronic cerebral circulatory failure). It has been established that Mildronate normalizes the tone and resistance of capillaries and arterioles of the brain, and restores their reactivity.

The effect of Mildronate on the rehabilitation process of patients with neurological disorders (after cerebrovascular diseases, brain surgery, tick-borne encephalitis) was studied.

The results of testing the therapeutic effectiveness indicate a positive, dose-dependent effect of the drug on the restoration of physical performance and functional independence of patients during the recovery period. When analyzing changes in individual and integral intellectual functions, a positive effect of Mildronate on the process of restoring intellectual functions during the rehabilitation period was revealed. It was found that Mildronate improves the quality of life of those recovering (mainly as a result of the restoration of physical functions), and also helps to eliminate mental disorders in patients.

During the rehabilitation period, Mildronate has a positive effect on the regression of nervous system dysfunction in patients with neurological deficits. The general neurological condition of patients improves (reduction of brain damage and reflex pathology, regression of paresis, improvement of motor coordination and autonomic functions).

In the clinic and practice of sports medicine, experimental data have been confirmed on the ability of Mildronate to increase performance and accelerate the processes of recovery after intense physical activity. These features of the drug’s action are characterized by improved tolerance to training loads, elimination of the feeling of fatigue, and a surge of vigor. In addition, the drug reduces emotional and mental stress (disappearance of apathy and irritability after exertion in training and competitions).

Toxicological characteristics

Mildronate is low toxic. When the active substance was administered orally to mice and rats, the LD50 value exceeded 18,000 mg/kg. Repeated administration of mildronate to rats and dogs for 6 months did not cause adverse changes in body weight, blood composition, biochemical parameters of blood and urine of animals. In high doses, Mildronate caused hemorrhages in the liver and kidneys in dogs, without affecting the functions of these organs.

When studying the specific toxicity of Mildronate, no teratogenic or embryotoxic effects were observed. The drug does not have mutagenic or carcinogenic properties. In experiments on animals, no allergenic effect was detected.