Metostabil 50 mg/ml

Indications

As part of combination therapy:

• anxiety states in neurotic and neurosis-like disorders;

• vegetative dystonia syndrome;

• chronic cerebral ischemia;

• mild cognitive disorders of atherosclerotic origin;

• acute cerebrovascular accidents (as part of combination therapy);

• withdrawal syndrome in alcoholism with predominance of neurosis-like and vegetative-vascular disorders (as part of combination therapy);

• in the treatment of acute intoxication with antipsychotic medications.

• traumatic brain injury, consequences of traumatic brain injuries.

• primary open-angle glaucoma of various stages, as part of combination therapy.

• as part of combination therapy for acute myocardial infarction.

Method of Administration and Dosage

The drug is administered intravenously (by bolus or infusion) or intramuscularly. For infusion, it is diluted in a 0.9% sodium chloride solution.
It is administered slowly by bolus over 5-7 minutes, or by infusion at a rate of 40-60 drops per minute. The maximum daily dose should not exceed 1200 mg.
In cases of acute cerebrovascular disorders in the first 10-14 days - intravenously by infusion at 200-500 mg 2-4 times a day, then intramuscularly at 200-250 mg 2-3 times a day for 2 weeks.
In cases of traumatic brain injury and its consequences for 10-15 days, intravenously by infusion at 200-500 mg 2-4 times a day.
In chronic cerebral ischemia in the decompensated stage, intravenously by bolus or infusion at a dose of 200-500 mg 1-2 times a day for 14 days. Then intramuscularly at 100-250 mg/day for 14 days.
In chronic ischemia, intramuscularly at 200-250 mg 2 times a day for 10-14 days.
In mild cognitive impairments in elderly patients and in anxiety disorders, intramuscularly at a daily dose of 100-300 mg for 14-30 days.
In the syndrome of vegetative dystonia, intramuscularly at 50-400 mg per day for 14 days.
In combination therapy for the treatment of withdrawal syndrome, intravenously by infusion or intramuscularly at 200-500 mg 2-3 times a day for 5-7 days. Treatment should be gradually discontinued, reducing the dose over 2-3 days.
In acute intoxication with antipsychotic agents, intravenously at a dose of 200-500 mg per day for 7-14 days.
In acute myocardial infarction, intravenously or intramuscularly for 14 days against the background of standard myocardial infarction therapy. In the first five days, for maximum effect, the drug should preferably be administered intravenously, and in the following 9 days intramuscularly. Intravenous administration is performed by drip infusion, slowly (to avoid side effects) in a 0.9% sodium chloride solution or 5% dextrose solution in a volume of 100-150 ml over 30-60 minutes. If necessary, slow bolus administration of the drug is possible, lasting at least 5 minutes. The drug is administered 3 times a day every 8 hours. The daily therapeutic dose is 6-9 mg/kg of body weight per day, with a single dose of 2-3 mg/kg. The maximum daily dose should not exceed 800 mg, with a single dose of 250 mg.
In glaucoma, intramuscularly at 100-300 mg/day for 14 days.

Composition per 1 ml:
Active ingredient: ethylmethylhydroxypyridine succinate - 50.0 mg.
Excipients: water for injections - up to 1.0 ml.

Description of the dosage form

colorless or slightly yellowish transparent liquid.

Section: Contraindications

• hypersensitivity to the drug;
• acute liver failure;
• acute kidney failure;
• childhood.

With caution - allergic diseases in history.

Special instructions

Pediatric use
The drug is not prescribed for children under 18 years of age due to insufficient study of the drug's effects.

Section: Side Effects

From the digestive system: nausea, dryness of the mucous membrane of the oral cavity or a metallic taste in the mouth, flatulence, diarrhea.
From the nervous system: drowsiness, difficulty falling asleep.
From the respiratory system: throat irritation, discomfort in the chest, feeling of shortness of breath (usually associated with excessively rapid administration and is of a short-term nature).
From the cardiovascular system: short-term increase in blood pressure.
Others: allergic reactions, sensation of "spreading warmth" throughout the body, unpleasant odor.

Section: Overdose

Due to low toxicity, overdose is unlikely. In case of accidental overdose, drowsiness and sedation may occur. Intravenous administration may lead to increased blood pressure (BP). Treatment is usually not required - symptoms resolve on their own within a day. In cases of excessive BP increase - antihypertensive medications under BP monitoring. In severe cases of insomnia - nitrazepam 10 mg, oxazepam 10 mg, or diazepam 5 mg.

Interaction

Enhances the effects of benzodiazepine anxiolytics, antiepileptic drugs (carbamazepine), and antiparkinsonian medications (levodopa).
Reduces the toxic effects of ethanol.

Pharmacodynamics

Ethylmethylhydroxypyridine succinate belongs to the class of 3-oxypyridines, is an inhibitor of free radical processes, and a membrane protector. It also has anti-hypoxic effects and increases the body's resistance to stress.
The mechanism of action of ethylmethylhydroxypyridine succinate is due to its antioxidant and membrane-protective effects. The drug inhibits lipid peroxidation, increases the activity of superoxide dismutase, enhances the lipid-protein ratio, and improves the structure and function of cell membranes.
Ethylmethylhydroxypyridine succinate modulates the activity of membrane-bound enzymes (calcium-independent phosphodiesterase, adenylate cyclase, acetylcholinesterase), receptor complexes (benzodiazepine, GABA, acetylcholine), which enhances their ability to bind with ligands, contributes to the preservation of the structural-functional organization of biomembranes, neurotransmitter transport, and improves synaptic transmission. Ethylmethylhydroxypyridine succinate increases dopamine levels in the brain. It causes an enhancement of compensatory activation of aerobic glycolysis and a reduction in the degree of inhibition of oxidative processes in the Krebs cycle under hypoxia, with an increase in ATP and creatine phosphate levels, and activates the energy-synthesizing functions of mitochondria.
It increases the body's resistance to various damaging factors in pathological conditions (hypoxia and ischemia, cerebrovascular disorders, ethanol intoxication, and antipsychotic medications).
In conditions of critically reduced coronary blood flow, it helps to preserve the structural-functional organization of cardiomyocyte membranes, stimulates the activity of membrane enzymes - phosphodiesterase, adenylate cyclase, acetylcholinesterase. It supports the activation of aerobic glycolysis that develops during acute ischemia and contributes to the restoration of mitochondrial redox processes under hypoxia, increasing ATP and creatine phosphate synthesis. It ensures the integrity of the morphological structures and physiological functions of ischemic myocardium. It improves the clinical course of myocardial infarction, increases the effectiveness of ongoing therapy, and reduces the frequency of arrhythmias and disturbances in intracardiac conduction.
It normalizes metabolic processes in ischemic myocardium, enhances the antianginal activity of nitrates, improves the rheological properties of blood, and reduces the consequences of reperfusion syndrome in acute coronary insufficiency.
It contributes to the preservation of ganglion cells of the retina and fibers of the optic nerve in progressive neuropathy caused by chronic ischemia and hypoxia. It improves the functional activity of the retina and optic nerve, increasing visual acuity.
It reduces enzymatic toxemia and endogenous intoxication in acute pancreatitis.
It improves metabolism and blood supply to the brain, microcirculation, and rheological properties of blood, reducing platelet aggregation. It stabilizes the membranes of blood cells (erythrocytes and platelets), reducing the likelihood of hemolysis. It has a hypolipidemic effect by reducing the levels of total cholesterol and low-density lipoproteins.

Pharmacokinetics

Absorption and Distribution

Upon single and course administration, the maximum concentration (Cmax) in plasma is reached in 0.58 hours. When administered at a dose of 400-500 mg, Cmax in plasma is 3.5-4 µg/ml. It is rapidly distributed in organs and tissues. The average retention time of ethylmethylhydroxypyridine succinate in the body is 0.7-1.3 hours.

Metabolism

It is metabolized in the liver by glucuronidation. Five metabolites have been identified: 3-hydroxypyridine phosphate - formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine; the second metabolite - pharmacologically active, is formed in large quantities and is found in urine 1-2 days after administration; the third - is excreted in large amounts in urine; the fourth and fifth - are glucuronoconjugates.

Excretion

It is rapidly eliminated from plasma and is practically undetectable after 4 hours. It is quickly excreted in urine mainly as metabolites (50% in 12 hours) and in small amounts in unchanged form (0.3% in 12 hours). The excretion rates of unchanged drug and metabolites in urine have individual variability.

Conditions of storage

Do not freeze.