Nitromax

INSTRUCTIONS FOR MEDICAL USE OF THE MEDICINAL PRODUCT NITROMAX (NITROMAX)

Composition:

Active substance: glyceryl trinitrate;

1 tablet contains 0.3 mg, 0.4 mg, or 0.5 mg of nitroglycerin;

Excipients: lactose monohydrate; potato starch; spherical sugar; crospovidone; magnesium stearate.

Pharmaceutical form. Sublingual tablets.

Main physicochemical properties: white or white with a yellowish tint tablets, with a flat surface, possibly rough.

Pharmacotherapeutic group.

Vasodilators used in cardiology. Organic nitrates. ATC code C01D A02.

Pharmacological Properties.

Pharmacodynamics.

Nitroglycerin is a peripheral vasodilator with a predominant effect on peripheral blood vessels.

Nitroglycerin acts directly on smooth muscle, primarily in venous and arterial vessels, via the nitrate receptor located in the smooth muscle layer of the vessel wall. In smooth muscle cells, nitroglycerin is enzymatically converted to produce nitric oxide (NO), which stimulates soluble guanylyl cyclase responsible for the formation of cyclic guanosine-3',5'-monophosphate (cGMP), a mediator of relaxation.

It affects central regulation of vascular tone and cardiac activity. It promotes the release of catecholamines in the brain and heart, resulting in central suppression of sympathetic and vasomotor tone, indirect sympathomimetic effects on the myocardium, and conformational changes in the troponin-tropomyosin complex. The nature and intensity of nitroglycerin's effects on the heart and peripheral vessels depend on the interaction between central and peripheral processes. Suppression of vasoconstrictor reflexes in coronary vessels, resulting from central inhibition of pain impulses, contributes to the relief of angina attacks. The antianginal effect of nitroglycerin is due to its normalizing influence on myocardial electrolyte and energy metabolism, particularly on key indicators of the respiratory chain—the ratio of oxidized to reduced forms of nicotinamide coenzymes and the activity of NAD-dependent dehydrogenases. It affects cardiac function and systemic hemodynamics. Under the influence of nitroglycerin, retrograde blood flow increases due to the dilation and increased number of functioning collaterals. Indirect sympathomimetic action, as well as accumulation of cyclic adenosine monophosphate (cAMP) in the myocardium, leads to enhanced contractility. Additionally, nitric oxide effectively inhibits both platelet aggregation and adhesion. Reduction in peripheral resistance and decreased venous return—effects associated with relaxation of vascular smooth muscles—lead to decreased preload and afterload on the heart. Venodilation reduces the volume of blood returning to the heart, thereby reducing preload, while arterial dilation reduces total peripheral resistance and afterload, ultimately reducing cardiac workload and improving coronary circulation.

Redistribution of myocardial blood flow occurs in favor of ischemic areas, and myocardial inotropic function is enhanced. Left ventricular end-diastolic pressure and heart size are reduced, improving blood supply to the subendocardial region of the myocardium, which is most vulnerable to ischemia. Reduction in peripheral venous and arterial resistance and cardiac filling pressure promotes decreased energy expenditure by the left ventricle and reduced myocardial oxygen demand. Pulmonary capillary pressure decreases, allowing nitroglycerin to be used in myocardial infarction complicated by pulmonary edema and in heart failure. In ischemic hypokinesia of specific myocardial regions, contractility is restored. Meningeal vessels dilate, while vessels of internal organs constrict; pulmonary arterial pressure decreases due to vasodilation and systemic effects of nitroglycerin. Nitroglycerin relaxes smooth muscles of the bronchi, biliary tract, gastrointestinal tract, and urinary tract. No teratogenic or embryotoxic effects were observed in experimental studies.

Pharmacokinetics.

After sublingual administration, the effect begins within 0.5–2 minutes; 75% of patients report improvement within the first 3 minutes, and another 15% within 4–15 minutes.

Sublingually administered nitroglycerin is absorbed through the mucous membrane and primarily enters the systemic circulation. Approximately 60–75% of the administered dose is absorbed. Maximum plasma concentration—2.3 µg/L—is reached within 2–4 minutes after administration; by the 8th minute, the concentration decreases by 50%, and nitroglycerin is almost undetectable in the blood by 20 minutes. It is rapidly metabolized in the liver. Nitrate esters of polyhydric alcohols undergo rapid denitration. Denitrated metabolites, such as 1,2- and 3,4-dinitrates, are less active but have a longer elimination half-life compared to nitroglycerin. The elimination half-life of nitroglycerin is approximately 30 minutes. Nitro groups are sequentially cleaved, both through the formation of inorganic nitrites and nitrates. From the organic portion of nitrate ester molecules, alcohols, aldehydes, and organic acids are formed. Four hours after administration, nitrate esters (initial compound) are almost undetectable. Nitrate esters are most actively metabolized in the liver, kidneys, and blood. They are cleaved via two pathways: by glutathione-dependent reductase, primarily located in the soluble fraction of hepatocytes, and by an enzyme that does not require reduced glutathione. The drug is primarily metabolized in the arterio-venous vascular bed, diffuses into smooth muscle cells, where it is converted into nitric oxide. A small portion of the drug, mainly under the influence of glutathione-S-reductase, is biotransformed in the liver into di- and mononitrates and glycerol. When administered orally, the majority of the drug undergoes hepatic metabolism ("first-pass effect"). A significant portion of dinitrate and mononitrate forms conjugates with glucuronic acid. Nitroglycerin metabolites are primarily excreted by the kidneys; some metabolites are eliminated via the lungs in exhaled air. Total clearance of nitroglycerin is 25–30 L.

Elimination half-life is 4–5 minutes. The elimination half-life of metabolites is 4 hours.

Clinical characteristics.

Indications.

Relief and short-term prophylaxis of angina attacks.

Contraindications.

Hypersensitivity to nitrates or excipients of the drug; cerebral ischemia, hemorrhagic stroke, intracranial hemorrhage, increased intracranial pressure, recent head trauma, bradycardia (less than 50 beats/min), arterial hypotension (systolic blood pressure below 100 mm Hg, diastolic blood pressure below 60 mm Hg), shock, collapse, hypertrophic obstructive cardiomyopathy, aortic stenosis, conditions associated with reduced left ventricular filling pressure (acute myocardial infarction, isolated mitral stenosis, constrictive pericarditis), cardiac tamponade, toxic pulmonary edema, closed-angle glaucoma with high intraocular pressure, concomitant use of phosphodiesterase-5 (PDE-5) inhibitors (sildenafil, tadalafil, vardenafil), severe anemia.

Interaction with other medicinal products and other forms of interaction.

Concomitant use with other vasodilators, antihypertensive agents, angiotensin-converting enzyme (ACE) inhibitors, "slow" calcium channel blockers, diuretics, neuroleptics, tricyclic antidepressants, sapropterin, monoamine oxidase inhibitors, ethanol and ethanol-containing preparations, beta-adrenoblockers, procainamides, acetylcysteine, quinidine, procainamide enhances the hypotensive effect of nitroglycerin.

Phosphodiesterase inhibitors (sildenafil, tadalafil, vardenafil) – concomitant use of nitroglycerin with these drugs is contraindicated due to the risk of uncontrolled arterial hypotension and life-threatening cardiovascular complications.

Tolerance to nitroglycerin may develop when used concomitantly with long-acting nitrate preparations.

Concomitant use with drugs causing dry mouth (anticholinergics, antimuscarinics, tricyclic antidepressants) reduces the efficacy of sublingual nitrates.

Concomitant sublingual administration of nitroglycerin and apomorphine may enhance the hypotensive effect.

Atropine and other drugs with M-cholinolytic action may reduce the effect of nitroglycerin due to decreased secretion and bioavailability of the drug.

Concomitant use with dihydroergotamine may lead to increased plasma concentration of dihydroergotamine and elevated blood pressure (due to increased bioavailability of dihydroergotamine).

Concomitant use with heparin may reduce heparin's anticoagulant effect (after discontinuation of the drug, a significant decrease in blood coagulation may occur, which may require dose reduction of heparin and early, frequent laboratory monitoring of blood coagulation).

Phenobarbital enhances nitrate metabolism in the liver. Alpha-adrenergic agonists, histamine, pituitrin, corticosteroids, central nervous system stimulants, bee and snake venom, and sunlight reduce the antianginal effect of nitroglycerin. Salicylates increase nitroglycerin blood levels; barbiturates accelerate its metabolism. Sulfhydryl group donors (captopril, acetylcysteine, unithiol) restore reduced sensitivity to nitroglycerin.

Special precautions.

Use with caution in patients with uncontrolled hypovolemia, heart failure with normal or low pulmonary arterial pressure, severe anemia, hyperthyroidism, hypoxemia, hypothermia, history of myocardial infarction, malnutrition, and severe renal and/or hepatic impairment (risk of developing methemoglobinemia).

Use with caution in patients with marked cerebral atherosclerosis and in elderly patients. Alcohol consumption is prohibited during treatment; visiting saunas, baths, and taking hot showers is contraindicated.

The tablet must not be chewed, as an excessive amount of the active substance may enter systemic circulation through the oral mucosa.

With frequent use, tolerance (tolerance development) may develop to nitroglycerin, as with other organic nitrates, requiring dose escalation. To prevent the development of tolerance during prolonged use, intermittent dosing throughout the day (with a 10–12 hour interval) or concomitant use of calcium antagonists, ACE inhibitors, or diuretics is recommended. If tolerance develops, temporary discontinuation of nitroglycerin (for several days) may be necessary, with substitution by antianginal agents from other pharmacotherapeutic groups.

Prior to first use of the drug, a physician consultation is required!

Patients must inform their physician about any previous reactions to medications of this group.

Significant reduction in arterial pressure and dizziness upon sudden change to an upright position from lying or sitting may occur during nitroglycerin use, especially when consuming alcohol, during physical exertion in hot weather.

If blurred vision or dry mouth persists or is pronounced, treatment must be discontinued.

Headache intensity associated with drug administration may be reduced by lowering the dose and/or concomitant use of valerian tincture (validol).

The risk of methemoglobinemia, manifested by cyanosis and blood discoloration, increases with prolonged uncontrolled use of nitroglycerin and administration of high doses in patients with hepatic insufficiency. In case of methemoglobinemia development, nitroglycerin must be urgently discontinued and an antidote administered—methylthioninium chloride (methylene blue). If continued nitrate therapy is necessary, methemoglobin levels must be monitored.

The drug contains lactose. If a patient has known sugar intolerance, a physician should be consulted before taking this medication.

Use during pregnancy or breastfeeding.

Use of NITROMAX during pregnancy or breastfeeding is contraindicated.

Ability to affect reaction rate when driving or operating machinery.

When driving vehicles or operating machinery requiring high concentration, it should be remembered that nitroglycerin intake may reduce reaction speed.

Dosage and Administration.

For angina pectoris, NITROMAX should be administered sublingually immediately after an attack occurs. The usual dose is 0.5 mg; however, a lower dose of 0.3 mg or 0.4 mg may be effective for many patients with stable angina. If no antianginal effect is observed within the first 5 minutes, another tablet should be taken.

If there is no therapeutic effect after administration of 1–1.5 mg of the drug, a physician must be called immediately (myocardial infarction is likely)!

NITROMAX acts for approximately 30 minutes. In cases of frequent angina attacks, prolonged-release formulations of nitroglycerin are recommended. However, if an angina attack occurs during treatment with prolonged-release nitrates, NITROMAX should be used to relieve the acute attack. Tolerance to sublingual nitrates develops rarely; however, if it occurs, the dose may need to be gradually increased in some patients up to 1.0–1.5 mg.

Children.

Experience with the use of this drug in children is limited; therefore, its use is not recommended in this age group.

Overdose.

Symptoms: decreased arterial blood pressure (below 90 mm Hg) with orthostatic dysregulation, headache, severe dizziness, fainting, tachycardia, cramps, diarrhea, nausea and vomiting, shortness of breath, pronounced weakness, drowsiness, elevated body temperature, sensation of warmth, arterial hypotension, increased sweating, chills.

When high doses are used (more than 20 mcg/kg): collapse, cyanosis of lips, nails or palms, methemoglobinemia, dyspnea and tachypnea.

Treatment: place the patient in a horizontal position with elevated lower limbs. In severe cases, administer plasma substitutes, sympathomimetics, and oxygen. In cases of methemoglobinemia, administer methylene blue, provided that the patient does not have glucose-6-phosphate dehydrogenase deficiency. Assess saturation. If saturation levels are low, administer oxygen therapy at a dose of 1–2 mg/kg body weight.

Adverse reactions.

Adverse reactions listed below have been reported during the use of the medicinal product.

Central nervous system: blurred vision, psychotic reactions, drowsiness, disorientation.

Gastrointestinal tract: dry mouth, abdominal pain.

Immune system: allergic reactions, including urticaria, itching; skin hyperemia, pallor, anaphylactic shock.

Other: excitement, visual disturbances, glaucoma exacerbation, hypothermia, sensation of heat.

Isolated cases of adverse reactions have also been reported: exacerbation of ischemic heart disease due to hypoxia, complete heart block, asystole, angioneurotic edema.

Shelf life.

2 years.

Storage conditions.

Store at a temperature not exceeding 30 °C in the original packaging.

Keep out of reach of children.

Packaging.

50 tablets in a light-protective glass bottle, 4 bottles in a cardboard box.

100 tablets in a light-protective glass bottle in a cardboard box.

50 tablets in a light-protective glass bottle, 3 bottles in a blister pack, 1 blister pack in a cardboard box.

50 tablets in a light-protective glass bottle, 3 bottles in a foil blister pack, 1 blister pack in a cardboard box.

Prescription status.

Over-the-counter.

Manufacturer.

MICROCHEM PHARMACEUTICAL COMPANY LTD (production unit (all stages of manufacturing process)).

Manufacturer's address and location of business activity.

33, Lenin Street, Rubizhne, Luhansk Oblast, 93000, Ukraine.

You can report an adverse event associated with the use of the medicinal product NITROMAX by calling +38 (050) 309-83-54 (24/7).

INSTRUCTION

for medical use of the medicinal product

NITROMAX

(NITROMAX)

Composition:

Active substance: glyceryl trinitrate;

1 tablet contains 0.3 mg, 0.4 mg, or 0.5 mg of nitroglycerin;

Excipients: lactose monohydrate; potato starch; spherical sugar; crospovidone; magnesium stearate.

Pharmaceutical form. Sublingual tablets.

Main physicochemical characteristics: white or off-white tablets, with a flat surface, possibly rough.

Pharmacotherapeutic group.

Vasodilators used in cardiology. Organic nitrates. ATC code C01D A02.

Pharmacological Properties

Pharmacodynamics

Nitroglycerin is a peripheral vasodilator with a predominant effect on peripheral blood vessels.

Nitroglycerin acts directly on smooth muscles, primarily of venous and arterial vessels, via the nitrate receptor located in the smooth muscle layer of the vessel wall. Enzymatically, nitroglycerin is converted within smooth muscle cells to nitric oxide (NO), which stimulates soluble guanylyl cyclase, leading to the formation of cyclic guanosine-3',5'-monophosphate (cGMP), the mediator of smooth muscle relaxation.

Nitroglycerin affects central regulation of vascular tone and cardiac activity. It promotes the release of catecholamines in the brain and heart, resulting in central suppression of sympathetic and vasomotor tone, indirect sympathomimetic effects on the myocardium, and conformational changes in the troponin-tropomyosin complex. The nature and intensity of nitroglycerin’s effects on the heart and peripheral vessels depend on the interaction between central and peripheral mechanisms. Suppression of vasoconstrictor reflexes in coronary vessels, resulting from central inhibition of pain impulses, contributes to relief of angina attacks. The antianginal effect of nitroglycerin is due to its normalizing influence on myocardial electrolyte and energy metabolism, particularly on key parameters of the respiratory chain—the ratio of oxidized to reduced forms of nicotinamide coenzymes and the activity of NAD-dependent dehydrogenases.

Nitroglycerin affects cardiac function and systemic hemodynamics. Under its influence, retrograde blood flow increases due to dilation and increased number of functioning collateral vessels. Indirect sympathomimetic action, as well as accumulation of cyclic adenosine monophosphate (cAMP) in the myocardium, leads to enhanced contractility. Additionally, nitric oxide effectively inhibits both platelet aggregation and adhesion.

Reduction in peripheral resistance and decreased venous return—effects associated with relaxation of vascular smooth muscles—result in decreased preload and afterload on the heart. Venodilation reduces the volume of blood returning to the heart, thereby decreasing preload, while arterial dilation reduces total peripheral resistance and afterload. Ultimately, this reduces cardiac workload and improves coronary circulation.

There is a redistribution of blood flow within the myocardium in favor of ischemic areas, and myocardial inotropic function is enhanced. End-diastolic pressure in the left ventricle and heart size are reduced, improving blood supply to the subendocardial region, which is most vulnerable to ischemia. Reduction in peripheral venous and arterial resistance and cardiac filling pressure contributes to decreased energy expenditure by the left ventricle and reduced myocardial oxygen demand. Pulmonary capillary pressure decreases, allowing nitroglycerin to be used in myocardial infarction complicated by pulmonary edema and in heart failure. In ischemic hypokinesia of specific myocardial regions, contractile function is restored.

Meningeal vessels dilate, while vessels of internal organs constrict. Pulmonary artery pressure decreases due to vasodilation and systemic effects of nitroglycerin. Nitroglycerin relaxes smooth muscles of the bronchi, biliary tract, gastrointestinal tract, and urinary tract. In experimental studies, no teratogenic or embryotoxic effects were observed.

Pharmacokinetics

After sublingual administration, the effect begins within 0.5–2 minutes; 75% of patients report improvement within the first 3 minutes, and another 15% within 4–15 minutes.

Sublingually administered nitroglycerin is absorbed through the mucous membrane and enters primarily into the systemic circulation. Approximately 60–75% of the administered dose is absorbed. Maximum plasma concentration—2.3 µg/L—is reached within 2–4 minutes after administration; by the 8th minute, the concentration decreases by 50%, and nitroglycerin is nearly undetectable in the blood within 20 minutes. It is rapidly metabolized in the liver. Nitrate esters of polyhydric alcohols undergo rapid denitration. Denitrated metabolites, such as 1,2- and 3,4-dinitrates, are less active but have a longer elimination half-life compared to nitroglycerin. The elimination half-life of nitroglycerin is approximately 30 minutes.

Nitro groups are sequentially cleaved both through formation of inorganic nitrites and nitrates. The organic portion of nitrate ester molecules yields alcohols, aldehydes, and organic acids. Four hours after administration, nitrate esters (initial compound) are nearly undetectable. The most active metabolism occurs in the liver, kidneys, and blood. Nitrate esters are degraded via two pathways: by glutathione-dependent reductase, primarily located in the soluble fraction of hepatocytes, and by an enzyme that does not require reduced glutathione.

The drug is primarily metabolized in the arterio-venous circulation, diffuses into smooth muscle cells, where it is converted into nitric oxide. A minor portion of the drug, mainly under the influence of glutathione-S-reductase, is biotransformed in the liver into di- and mononitrates and glycerol. When administered orally, the majority of the drug undergoes hepatic metabolism (first-pass effect). A significant portion of dinitrate and mononitrate metabolites form conjugates with glucuronic acid. Metabolites of nitroglycerin are primarily excreted by the kidneys; some metabolites are eliminated via the lungs in exhaled air. Total clearance of nitroglycerin is 25–30 L.

Elimination half-life is 4–5 minutes. Elimination half-life of metabolites is 4 hours.

Clinical characteristics.

Indications.

Relief and short-term prevention of angina attacks.

Contraindications.

Hypersensitivity to nitrates and excipients of the medicinal product; cerebral ischemia, hemorrhagic stroke, intracranial hemorrhage, increased intracranial pressure, recent head trauma, bradycardia (less than 50 beats/min), arterial hypotension (systolic blood pressure below 100 mm Hg, diastolic blood pressure below 60 mm Hg), shock, collapse, hypertrophic obstructive cardiomyopathy, aortic stenosis, conditions associated with reduced left ventricular filling pressure (acute myocardial infarction, isolated mitral stenosis, constrictive pericarditis), cardiac tamponade, toxic pulmonary edema, closed-angle glaucoma with high intraocular pressure, concomitant use of phosphodiesterase-5 (PDE-5) inhibitors (sildenafil, tadalafil, vardenafil), severe anemia.

Interaction with other medicinal products and other types of interactions.

When used concomitantly with other vasodilators, antihypertensive agents, angiotensin-converting enzyme (ACE) inhibitors, "slow" calcium channel blockers, diuretics, neuroleptics, tricyclic antidepressants, sapropterin, monoamine oxidase inhibitors, ethanol and ethanol-containing preparations, beta-adrenoblockers, procainamides, acetylcysteine, quinidine, and procainamide, the hypotensive effect of nitroglycerin is enhanced.

Phosphodiesterase inhibitors (sildenafil, tadalafil, vardenafil) – concomitant use of nitroglycerin with these drugs is contraindicated due to the risk of uncontrolled arterial hypotension and life-threatening cardiovascular complications.

Tolerance to nitroglycerin may develop when used concomitantly with long-acting nitrate preparations.

Concomitant use with drugs causing dry mouth (anticholinergics, antimuscarinics, tricyclic antidepressants) may reduce the efficacy of sublingual nitrates.

Simultaneous sublingual administration of nitroglycerin and apomorphine may enhance the hypotensive effect.

Atropine and other drugs exhibiting M-cholinolytic activity may reduce the effect of nitroglycerin due to decreased secretion and bioavailability of the drug.

Concomitant use with dihydroergotamine may lead to increased plasma concentration of dihydroergotamine and elevated blood pressure (due to increased bioavailability of dihydroergotamine).

When used concomitantly with heparin, the anticoagulant effect of heparin may be reduced (after discontinuation of the drug, a significant decrease in blood coagulation may occur, which may require dose reduction of heparin and early, frequent laboratory monitoring of blood coagulation).

Phenobarbital enhances the metabolism of nitrates in the liver. Alpha-adrenergic agonists, histamine, pituitrin, corticosteroids, central nervous system stimulants, bee and snake venom, and sunlight reduce the antianginal effect of nitroglycerin. Salicylates increase the level of nitroglycerin in blood, while barbiturates accelerate its metabolism. Sulfhydryl group donors (captopril, acetylcysteine, unithiol) restore reduced sensitivity to nitroglycerin.

Special precautions.

Use with caution in patients with uncontrolled hypovolemia, heart failure with normal or low pulmonary arterial pressure, severe anemia, hyperthyroidism, hypoxemia, hypothermia, history of myocardial infarction, malnutrition, and severe renal and/or hepatic impairment (risk of developing methemoglobinemia).

Use with caution in patients with marked cerebral atherosclerosis and in elderly patients. During treatment, alcohol consumption is not permitted; visiting saunas, steam baths, and taking hot showers is contraindicated.

The tablet must not be chewed, as an excessive amount of the active substance may enter systemic circulation through the oral mucosa.

With frequent use, tolerance (tolerance development) may develop to nitroglycerin, as with other organic nitrates, requiring dose escalation. To prevent the development of tolerance during prolonged use, intermittent dosing within a 24-hour period (with a 10–12 hour interval) is recommended, or concomitant use of calcium antagonists, ACE inhibitors, or diuretics. If tolerance develops, temporary discontinuation of nitroglycerin (for several days) may be necessary, with substitution by antianginal agents from other pharmacotherapeutic groups.

Prior to first use of the drug, consultation with a physician is required!

The patient must inform the physician about any previous reaction to medications of this group.

When taking nitroglycerin, a significant drop in arterial blood pressure and dizziness may occur upon sudden transition from a lying or sitting position to an upright position, when consuming alcohol, or during physical exertion in hot weather.

If blurred vision or dry mouth persists or is pronounced, treatment must be discontinued.

The intensity of headache associated with drug intake may be reduced by lowering the dose and/or concomitant use of valeridine (validol).

The risk of methemoglobinemia, manifested by cyanosis and blood discoloration, increases with prolonged uncontrolled use of nitroglycerin and with high-dose administration in patients with hepatic insufficiency. In case of methemoglobinemia development, nitroglycerin must be urgently discontinued and an antidote administered—methylene blue (methylthioninium chloride). If continued nitrate therapy is required, methemoglobin levels must be monitored.

The drug contains lactose. If the patient has a diagnosed sugar intolerance, medical advice must be sought before taking this medicinal product.

Use during pregnancy or breastfeeding.

Use of NITROMAX during pregnancy or breastfeeding is contraindicated.

Ability to affect reaction rate when driving or operating machinery.

When driving vehicles or operating machinery requiring high concentration and rapid reactions, it should be remembered that nitroglycerin intake may reduce reaction speed.

Dosage and Administration

For angina pectoris, NITROMAX should be administered sublingually immediately after the onset of an attack. The usual dose is 0.5 mg; however, a lower dose of 0.3 mg or 0.4 mg may be effective for many patients with stable angina. If no antianginal effect occurs within the first 5 minutes, another tablet should be taken.

If there is no therapeutic response after administration of 1–1.5 mg of the drug, a physician must be called immediately (myocardial infarction is likely)!

NITROMAX acts for approximately 30 minutes. In cases of frequent angina attacks, prolonged-release formulations of nitroglycerin are recommended. However, if an angina attack occurs during treatment with prolonged-release nitrates, NITROMAX should be used to relieve the acute episode. Tolerance to sublingual nitrates develops rarely, but if it occurs, the dose may need to be gradually increased in some patients up to 1.0–1.5 mg.

Children

Experience with the use of this drug in children is limited; therefore, its use is not recommended in this age group.

Overdose

Symptoms: reduction in arterial blood pressure (below 90 mm Hg) with orthostatic dysregulation, headache, severe dizziness, syncope, tachycardia, colic, diarrhea, nausea and vomiting, dyspnea, marked weakness, somnolence, elevated body temperature, sensation of warmth, arterial hypotension, increased sweating, chills.

With high doses (more than 20 mcg/kg): collapse, cyanosis of lips, nails or palms, methemoglobinemia, dyspnea, and tachypnea.

Treatment: place the patient in a horizontal position with legs elevated. In severe cases, administer plasma expanders, sympathomimetics, and oxygen. In cases of methemoglobinemia, administer methylene blue, provided the patient does not have glucose-6-phosphate dehydrogenase deficiency. Assess saturation. If saturation levels indicate a need, oxygen therapy should be administered at a dose of 1–2 mg/kg body weight.

Side effects.

The following adverse reactions have been reported during the use of the medicinal product.

Central nervous system: blurred vision, psychotic reactions, drowsiness, disorientation.

Gastrointestinal tract: dry mouth, abdominal pain.

Immune system: allergic reactions, including urticaria, pruritus; skin hyperemia, pallor, anaphylactic shock.

Other: excitability, visual disturbances, glaucoma exacerbation, hypothermia, sensation of heat.

Isolated cases of adverse reactions have also been reported: exacerbation of ischemic heart disease due to hypoxia, complete heart block, asystole, angioneurotic edema.

Shelf life.

2 years.

Storage conditions.

Store at a temperature not exceeding 30 °C in the original packaging.

Keep out of reach of children.

Packaging.

50 tablets in a light-protected glass bottle, 4 bottles in a cardboard box.

100 tablets in a light-protected glass bottle in a cardboard box.

50 tablets in a light-protected glass bottle, 3 bottles in a blister pack, 1 blister pack in a cardboard box.

50 tablets in a light-protected glass bottle, 3 bottles in a foil blister pack, 1 blister pack in a cardboard box.

Prescription status.

Over-the-counter.

Manufacturer.

MICROCHEM LLC (responsible for batch release, excluding batch control/testing).

Manufacturer's address and location of business activity.

5 Budynstriji Str., Kyiv, Ukraine, 01013

You can report an adverse event associated with this medicinal product at +38 (050) 309-83-54 (24/7).