MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. (Ethylmethylhydroxypyridine succinate, Pyridoxine)
Special Price
$23.80
Regular Price
$28.00
In stock
SKU
newyork487342
Pharmacological action
Farmgroup:
Antioxidant + vitamin.
Pharmacological action:
MeksiV 6В® - the combined preparation.
- Ethylmethylhydroxypyridine succinate inhibitor of free radical processes - a membrane protector that also has antihypoxic, stress-protective, nootropic, antiepileptic and anxiolytic effects. An antioxidant drug that regulates metabolic processes in the myocardium and vascular wall.
The mechanism of action is due to antioxidant and membrane-protective properties. It suppresses lipid peroxidation, increases the activity of superoxide oxidase, increases the lipid-protein ratio, improves the structure and function of cell membranes. Modulates the activity of membrane-bound enzymes, receptor complexes, which helps preserve the structural and functional organization of biomembranes, transport of neurotransmitters and improve synaptic transmission. Increases dopamine concentration in the brain.
Enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxia with an increase in adenositriphosphoric acid (ATP) and creatine phosphate, and activates the energy-synthesizing function of mitochondria.
Increases the body's resistance to various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accident, intoxication with ethanol and antipsychotic drugs).
Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (red blood cells and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and low density lipoproteins (LDL).
Improves the functional state of the ischemic myocardium, reducing the manifestations of systolic and diastolic dysfunction of the left ventricle (LV), as well as electrical myocardial instability.
In conditions of a critical decrease in coronary blood flow, it helps to maintain the structural and functional organization of the membranes of cardiomyocytes, stimulates the activity of membrane enzymes - phosphodiesterase, adenylate cyclase, acetylcholinesterase. It supports the activation of aerobic glycolysis that develops in acute ischemia and, under hypoxic conditions, promotes the restoration of mitochondrial redox processes, increases the synthesis of adenositriphosphoric acid (ATP), creatine phosphate and other macroergs. It increases collateral blood supply to the ischemic myocardium and activates energy-synthesizing processes in the ischemic zone, which helps to preserve the integrity of cardiomyocytes and maintain their functional activity.
In patients with stable angina, stress increases exercise tolerance and antianginal activity of nitrates, improves blood rheology, and reduces the incidence of acute coronary insufficiency.
- Pyridoxine, when ingested, is phosphorylated, converted to pyridoxal-5-phosphate and is part of enzymes that decarboxylate, transamine and racemize amino acids, as well as the enzymatic conversion of sulfur-containing and hydroxylated amino acids. Participates in the metabolism necessary for the normal functioning of the central and peripheral nervous system. Pyridoxine is involved in the metabolism of tryptophan, methionine, cysteine, glutamine and other amino acids. It plays an important role in the exchange of histamine. Helps normalize lipid metabolism.
Pharmacokinetics:
Ethylmethylhydroxypyridine succinate is rapidly absorbed by ingestion (half-absorption period - 0.08–1 h). The time to reach the maximum concentration (Tcmax) when taken orally is 0.46–0.5 hours. The maximum concentration (Cmax) when taken orally is 50–100 ng / ml. It is quickly distributed in organs and tissues. The average retention time of ethylmethylhydroxypyridine succinate in the body when taken orally is 4.9–5.2 hours.
Ethyl methylhydroxypyridine succinate is metabolized in the liver by glucuronidation. 5 metabolites have been identified: 3-hydroxypyridine phosphate - is formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine. The 2nd metabolite is pharmacologically active, is formed in large quantities and is found in urine 1–2 days after the 3rd it is excreted in in large quantities with urine 4th and 5th - glucuronconjugates. The half-life when ingested is 4.7–5 hours. It is rapidly excreted in the urine mainly in the form of metabolites (50% in 12 hours) and in insignificant amounts unchanged (0.3% in 12 hours). It is most intensively excreted during the first 4 hours after taking ethylmethylhydroxypyridine succinate. The urinary excretion rates of unchanged ethylmethylhydroxypyridine succinate and metabolites have significant individual variability.
Pyridoxine is rapidly absorbed throughout the small intestine, a larger amount is absorbed in the jejunum. It is metabolized in the liver with the formation of pharmacologically active metabolites (pyridoxal phosphate and pyridoxamine phosphate). Pyridoxal phosphate bound to plasma proteins by 90%. It penetrates well into all tissues, accumulates mainly in the liver, less - in the muscles and central nervous system (CNS). It penetrates the placenta, is secreted with breast milk. The elimination half-life (T1 / 2) is 15–20 days. It is excreted by the kidneys (with intravenous administration - with bile 2%), as well as during hemodialysis. Buy MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. (Ethylmethylhydroxypyridine succinate, Pyridoxine) in newyork free shipping. Fast international shipping USA, AU, EU, UK and others.
Farmgroup:
Antioxidant + vitamin.
Pharmacological action:
MeksiV 6В® - the combined preparation.
- Ethylmethylhydroxypyridine succinate inhibitor of free radical processes - a membrane protector that also has antihypoxic, stress-protective, nootropic, antiepileptic and anxiolytic effects. An antioxidant drug that regulates metabolic processes in the myocardium and vascular wall.
The mechanism of action is due to antioxidant and membrane-protective properties. It suppresses lipid peroxidation, increases the activity of superoxide oxidase, increases the lipid-protein ratio, improves the structure and function of cell membranes. Modulates the activity of membrane-bound enzymes, receptor complexes, which helps preserve the structural and functional organization of biomembranes, transport of neurotransmitters and improve synaptic transmission. Increases dopamine concentration in the brain.
Enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxia with an increase in adenositriphosphoric acid (ATP) and creatine phosphate, and activates the energy-synthesizing function of mitochondria.
Increases the body's resistance to various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accident, intoxication with ethanol and antipsychotic drugs).
Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (red blood cells and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and low density lipoproteins (LDL).
Improves the functional state of the ischemic myocardium, reducing the manifestations of systolic and diastolic dysfunction of the left ventricle (LV), as well as electrical myocardial instability.
In conditions of a critical decrease in coronary blood flow, it helps to maintain the structural and functional organization of the membranes of cardiomyocytes, stimulates the activity of membrane enzymes - phosphodiesterase, adenylate cyclase, acetylcholinesterase. It supports the activation of aerobic glycolysis that develops in acute ischemia and, under hypoxic conditions, promotes the restoration of mitochondrial redox processes, increases the synthesis of adenositriphosphoric acid (ATP), creatine phosphate and other macroergs. It increases collateral blood supply to the ischemic myocardium and activates energy-synthesizing processes in the ischemic zone, which helps to preserve the integrity of cardiomyocytes and maintain their functional activity.
In patients with stable angina, stress increases exercise tolerance and antianginal activity of nitrates, improves blood rheology, and reduces the incidence of acute coronary insufficiency.
- Pyridoxine, when ingested, is phosphorylated, converted to pyridoxal-5-phosphate and is part of enzymes that decarboxylate, transamine and racemize amino acids, as well as the enzymatic conversion of sulfur-containing and hydroxylated amino acids. Participates in the metabolism necessary for the normal functioning of the central and peripheral nervous system. Pyridoxine is involved in the metabolism of tryptophan, methionine, cysteine, glutamine and other amino acids. It plays an important role in the exchange of histamine. Helps normalize lipid metabolism.
Pharmacokinetics:
Ethylmethylhydroxypyridine succinate is rapidly absorbed by ingestion (half-absorption period - 0.08–1 h). The time to reach the maximum concentration (Tcmax) when taken orally is 0.46–0.5 hours. The maximum concentration (Cmax) when taken orally is 50–100 ng / ml. It is quickly distributed in organs and tissues. The average retention time of ethylmethylhydroxypyridine succinate in the body when taken orally is 4.9–5.2 hours.
Ethyl methylhydroxypyridine succinate is metabolized in the liver by glucuronidation. 5 metabolites have been identified: 3-hydroxypyridine phosphate - is formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine. The 2nd metabolite is pharmacologically active, is formed in large quantities and is found in urine 1–2 days after the 3rd it is excreted in in large quantities with urine 4th and 5th - glucuronconjugates. The half-life when ingested is 4.7–5 hours. It is rapidly excreted in the urine mainly in the form of metabolites (50% in 12 hours) and in insignificant amounts unchanged (0.3% in 12 hours). It is most intensively excreted during the first 4 hours after taking ethylmethylhydroxypyridine succinate. The urinary excretion rates of unchanged ethylmethylhydroxypyridine succinate and metabolites have significant individual variability.
Pyridoxine is rapidly absorbed throughout the small intestine, a larger amount is absorbed in the jejunum. It is metabolized in the liver with the formation of pharmacologically active metabolites (pyridoxal phosphate and pyridoxamine phosphate). Pyridoxal phosphate bound to plasma proteins by 90%. It penetrates well into all tissues, accumulates mainly in the liver, less - in the muscles and central nervous system (CNS). It penetrates the placenta, is secreted with breast milk. The elimination half-life (T1 / 2) is 15–20 days. It is excreted by the kidneys (with intravenous administration - with bile 2%), as well as during hemodialysis. Buy MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. (Ethylmethylhydroxypyridine succinate, Pyridoxine) in newyork free shipping. Fast international shipping USA, AU, EU, UK and others.
Pharmacological action
Farmgroup:
Antioxidant + vitamin.
Pharmacological action:
MeksiV 6В® - the combined preparation.
- Ethylmethylhydroxypyridine succinate inhibitor of free radical processes - a membrane protector that also has antihypoxic, stress-protective, nootropic, antiepileptic and anxiolytic effects. An antioxidant drug that regulates metabolic processes in the myocardium and vascular wall.
The mechanism of action is due to antioxidant and membrane-protective properties. It suppresses lipid peroxidation, increases the activity of superoxide oxidase, increases the lipid-protein ratio, improves the structure and function of cell membranes. Modulates the activity of membrane-bound enzymes, receptor complexes, which helps preserve the structural and functional organization of biomembranes, transport of neurotransmitters and improve synaptic transmission. Increases dopamine concentration in the brain.
Enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxia with an increase in adenositriphosphoric acid (ATP) and creatine phosphate, and activates the energy-synthesizing function of mitochondria.
Increases the body's resistance to various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accident, intoxication with ethanol and antipsychotic drugs).
Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (red blood cells and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and low density lipoproteins (LDL).
Improves the functional state of the ischemic myocardium, reducing the manifestations of systolic and diastolic dysfunction of the left ventricle (LV), as well as electrical myocardial instability.
In conditions of a critical decrease in coronary blood flow, it helps to maintain the structural and functional organization of the membranes of cardiomyocytes, stimulates the activity of membrane enzymes - phosphodiesterase, adenylate cyclase, acetylcholinesterase. It supports the activation of aerobic glycolysis that develops in acute ischemia and, under hypoxic conditions, promotes the restoration of mitochondrial redox processes, increases the synthesis of adenositriphosphoric acid (ATP), creatine phosphate and other macroergs. It increases collateral blood supply to the ischemic myocardium and activates energy-synthesizing processes in the ischemic zone, which helps to preserve the integrity of cardiomyocytes and maintain their functional activity.
In patients with stable angina, stress increases exercise tolerance and antianginal activity of nitrates, improves blood rheology, and reduces the incidence of acute coronary insufficiency.
- Pyridoxine, when ingested, is phosphorylated, converted to pyridoxal-5-phosphate and is part of enzymes that decarboxylate, transamine and racemize amino acids, as well as the enzymatic conversion of sulfur-containing and hydroxylated amino acids. Participates in the metabolism necessary for the normal functioning of the central and peripheral nervous system. Pyridoxine is involved in the metabolism of tryptophan, methionine, cysteine, glutamine and other amino acids. It plays an important role in the exchange of histamine. Helps normalize lipid metabolism.
Pharmacokinetics:
Ethylmethylhydroxypyridine succinate is rapidly absorbed by ingestion (half-absorption period - 0.08–1 h). The time to reach the maximum concentration (Tcmax) when taken orally is 0.46–0.5 hours. The maximum concentration (Cmax) when taken orally is 50–100 ng / ml. It is quickly distributed in organs and tissues. The average retention time of ethylmethylhydroxypyridine succinate in the body when taken orally is 4.9–5.2 hours.
Ethyl methylhydroxypyridine succinate is metabolized in the liver by glucuronidation. 5 metabolites have been identified: 3-hydroxypyridine phosphate - is formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine. The 2nd metabolite is pharmacologically active, is formed in large quantities and is found in urine 1–2 days after the 3rd it is excreted in in large quantities with urine 4th and 5th - glucuronconjugates. The half-life when ingested is 4.7–5 hours. It is rapidly excreted in the urine mainly in the form of metabolites (50% in 12 hours) and in insignificant amounts unchanged (0.3% in 12 hours). It is most intensively excreted during the first 4 hours after taking ethylmethylhydroxypyridine succinate. The urinary excretion rates of unchanged ethylmethylhydroxypyridine succinate and metabolites have significant individual variability.
Pyridoxine is rapidly absorbed throughout the small intestine, a larger amount is absorbed in the jejunum. It is metabolized in the liver with the formation of pharmacologically active metabolites (pyridoxal phosphate and pyridoxamine phosphate). Pyridoxal phosphate bound to plasma proteins by 90%. It penetrates well into all tissues, accumulates mainly in the liver, less - in the muscles and central nervous system (CNS). It penetrates the placenta, is secreted with breast milk. The elimination half-life (T1 / 2) is 15–20 days. It is excreted by the kidneys (with intravenous administration - with bile 2%), as well as during hemodialysis.
Indications
As part of combination therapy: - vascular encephalopathy
- syndrome vegetative dystonia
- tpevozhnyh states DURING nevpoticheskix and nevpozopodobnyx sostoyaniyah
- abstinentnogo sindpoma DURING alkogolizme with ppeobladaniem nevpozopodobnyx and vegetativno-sosudistyx rasstpoystv
- coronary heart disease (seizure prevention)
- soctoyaniya posle ostpoy intoksikatsii antipsixoticheskimi spedstvami
- asthenic conditions, as well as for the prevention of the development of somatic diseases due to the impact of extreme factors and loading
- the impact of extreme (stress).
Contraindications
Hypersensitivity
acute liver and / or renal failure
pregnancy, lactation, childhood.
Caution: Peptic ulcer and 12 duodenal ulcer.
Composition
1 tablet: - ethylmethylhydroxypyridine succinate 125 mg
- pyridoxine hydrochloride 10 mg
excipients:
calcium hydrogen phosphate dihydrate, copovidone (sirdlid 6-cordidone 6-pyrididone 6 Collidone colloidal (aerosil), croscarmellose sodium
(primellose), magnesium lrdate
, magnesium stearate,
hydrogenated castor oil,
microcrystalline cellulose
film composition:
Selecout AQ-02003 [hypromellose (hydroxypropylmethyl cellulose),
macrogol (6000 polyethylene glycol), titanium.
Dosage and administration
Inside, 1 tablet of Mexib 6 3 times a day, the initial dose of 1-2 tablets 1-2 times a day with a gradual increase to obtain a therapeutic effect.
The maximum daily dose of Mexico is 6 to 6 tablets per day. The duration of treatment is 2-8 weeks.
If necessary, repeated courses are possible.
Side effects
Nausea, dry mouth, diarrhea, drowsiness, allergic reactions, hypersecretion of hydrochloric acid (HCl), numbness, a feeling of compression in the extremities - a symptom of “stocking” and “gloves”, a decrease in lactation (sometimes it is used as a treatment the effect).
Overdose
Symptoms: sleep disturbances (insomnia, in some cases drowsiness).
Treatment, as a rule, is not required - the symptoms disappear on their own within a day. In severe cases with insomnia, nitrazepam 10 mg, oxazepam 10 mg or diazepam 5 mg.
Active ingredient
Ethylmethylhydroxypyridine succinate, Pyridoxine
pharmacy terms and conditions without a prescription
lekarstvennaja form
tablets
Appointment by a doctor, Children older than 3 years, For adults, Feeding mothers13
Adult doctor
Indications
From concussion and other traumatic brain injuries, From atherosclerosis, From exposure to adverse factors, From stress, From asthenia, From a hangover, From vegetative-vascular disorders, From p the effects of stroke, From neurosis, From cerebrovascular accident
Kanonfarma, Russia
MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. (Ethylmethylhydroxypyridine succinate, Pyridoxine) florida in pharmacy online. Cheap price, instruction, side effects, dosage. MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. - Sale. PayPal accept. Free shipping florida. Fast international shipping.
Farmgroup:
Antioxidant + vitamin.
Pharmacological action:
MeksiV 6В® - the combined preparation.
- Ethylmethylhydroxypyridine succinate inhibitor of free radical processes - a membrane protector that also has antihypoxic, stress-protective, nootropic, antiepileptic and anxiolytic effects. An antioxidant drug that regulates metabolic processes in the myocardium and vascular wall.
The mechanism of action is due to antioxidant and membrane-protective properties. It suppresses lipid peroxidation, increases the activity of superoxide oxidase, increases the lipid-protein ratio, improves the structure and function of cell membranes. Modulates the activity of membrane-bound enzymes, receptor complexes, which helps preserve the structural and functional organization of biomembranes, transport of neurotransmitters and improve synaptic transmission. Increases dopamine concentration in the brain.
Enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxia with an increase in adenositriphosphoric acid (ATP) and creatine phosphate, and activates the energy-synthesizing function of mitochondria.
Increases the body's resistance to various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accident, intoxication with ethanol and antipsychotic drugs).
Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (red blood cells and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and low density lipoproteins (LDL).
Improves the functional state of the ischemic myocardium, reducing the manifestations of systolic and diastolic dysfunction of the left ventricle (LV), as well as electrical myocardial instability.
In conditions of a critical decrease in coronary blood flow, it helps to maintain the structural and functional organization of the membranes of cardiomyocytes, stimulates the activity of membrane enzymes - phosphodiesterase, adenylate cyclase, acetylcholinesterase. It supports the activation of aerobic glycolysis that develops in acute ischemia and, under hypoxic conditions, promotes the restoration of mitochondrial redox processes, increases the synthesis of adenositriphosphoric acid (ATP), creatine phosphate and other macroergs. It increases collateral blood supply to the ischemic myocardium and activates energy-synthesizing processes in the ischemic zone, which helps to preserve the integrity of cardiomyocytes and maintain their functional activity.
In patients with stable angina, stress increases exercise tolerance and antianginal activity of nitrates, improves blood rheology, and reduces the incidence of acute coronary insufficiency.
- Pyridoxine, when ingested, is phosphorylated, converted to pyridoxal-5-phosphate and is part of enzymes that decarboxylate, transamine and racemize amino acids, as well as the enzymatic conversion of sulfur-containing and hydroxylated amino acids. Participates in the metabolism necessary for the normal functioning of the central and peripheral nervous system. Pyridoxine is involved in the metabolism of tryptophan, methionine, cysteine, glutamine and other amino acids. It plays an important role in the exchange of histamine. Helps normalize lipid metabolism.
Pharmacokinetics:
Ethylmethylhydroxypyridine succinate is rapidly absorbed by ingestion (half-absorption period - 0.08–1 h). The time to reach the maximum concentration (Tcmax) when taken orally is 0.46–0.5 hours. The maximum concentration (Cmax) when taken orally is 50–100 ng / ml. It is quickly distributed in organs and tissues. The average retention time of ethylmethylhydroxypyridine succinate in the body when taken orally is 4.9–5.2 hours.
Ethyl methylhydroxypyridine succinate is metabolized in the liver by glucuronidation. 5 metabolites have been identified: 3-hydroxypyridine phosphate - is formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine. The 2nd metabolite is pharmacologically active, is formed in large quantities and is found in urine 1–2 days after the 3rd it is excreted in in large quantities with urine 4th and 5th - glucuronconjugates. The half-life when ingested is 4.7–5 hours. It is rapidly excreted in the urine mainly in the form of metabolites (50% in 12 hours) and in insignificant amounts unchanged (0.3% in 12 hours). It is most intensively excreted during the first 4 hours after taking ethylmethylhydroxypyridine succinate. The urinary excretion rates of unchanged ethylmethylhydroxypyridine succinate and metabolites have significant individual variability.
Pyridoxine is rapidly absorbed throughout the small intestine, a larger amount is absorbed in the jejunum. It is metabolized in the liver with the formation of pharmacologically active metabolites (pyridoxal phosphate and pyridoxamine phosphate). Pyridoxal phosphate bound to plasma proteins by 90%. It penetrates well into all tissues, accumulates mainly in the liver, less - in the muscles and central nervous system (CNS). It penetrates the placenta, is secreted with breast milk. The elimination half-life (T1 / 2) is 15–20 days. It is excreted by the kidneys (with intravenous administration - with bile 2%), as well as during hemodialysis.
Indications
As part of combination therapy: - vascular encephalopathy
- syndrome vegetative dystonia
- tpevozhnyh states DURING nevpoticheskix and nevpozopodobnyx sostoyaniyah
- abstinentnogo sindpoma DURING alkogolizme with ppeobladaniem nevpozopodobnyx and vegetativno-sosudistyx rasstpoystv
- coronary heart disease (seizure prevention)
- soctoyaniya posle ostpoy intoksikatsii antipsixoticheskimi spedstvami
- asthenic conditions, as well as for the prevention of the development of somatic diseases due to the impact of extreme factors and loading
- the impact of extreme (stress).
Contraindications
Hypersensitivity
acute liver and / or renal failure
pregnancy, lactation, childhood.
Caution: Peptic ulcer and 12 duodenal ulcer.
Composition
1 tablet: - ethylmethylhydroxypyridine succinate 125 mg
- pyridoxine hydrochloride 10 mg
excipients:
calcium hydrogen phosphate dihydrate, copovidone (sirdlid 6-cordidone 6-pyrididone 6 Collidone colloidal (aerosil), croscarmellose sodium
(primellose), magnesium lrdate
, magnesium stearate,
hydrogenated castor oil,
microcrystalline cellulose
film composition:
Selecout AQ-02003 [hypromellose (hydroxypropylmethyl cellulose),
macrogol (6000 polyethylene glycol), titanium.
Dosage and administration
Inside, 1 tablet of Mexib 6 3 times a day, the initial dose of 1-2 tablets 1-2 times a day with a gradual increase to obtain a therapeutic effect.
The maximum daily dose of Mexico is 6 to 6 tablets per day. The duration of treatment is 2-8 weeks.
If necessary, repeated courses are possible.
Side effects
Nausea, dry mouth, diarrhea, drowsiness, allergic reactions, hypersecretion of hydrochloric acid (HCl), numbness, a feeling of compression in the extremities - a symptom of “stocking” and “gloves”, a decrease in lactation (sometimes it is used as a treatment the effect).
Overdose
Symptoms: sleep disturbances (insomnia, in some cases drowsiness).
Treatment, as a rule, is not required - the symptoms disappear on their own within a day. In severe cases with insomnia, nitrazepam 10 mg, oxazepam 10 mg or diazepam 5 mg.
Active ingredient
Ethylmethylhydroxypyridine succinate, Pyridoxine
pharmacy terms and conditions without a prescription
lekarstvennaja form
tablets
Appointment by a doctor, Children older than 3 years, For adults, Feeding mothers13
Adult doctor
Indications
From concussion and other traumatic brain injuries, From atherosclerosis, From exposure to adverse factors, From stress, From asthenia, From a hangover, From vegetative-vascular disorders, From p the effects of stroke, From neurosis, From cerebrovascular accident
Kanonfarma, Russia
MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. (Ethylmethylhydroxypyridine succinate, Pyridoxine) florida in pharmacy online. Cheap price, instruction, side effects, dosage. MeksiV 6 tablets it is covered. 125mg + 10mg 30 pcs. - Sale. PayPal accept. Free shipping florida. Fast international shipping.
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