Nitroglycerin

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

Composition:

Active substance: glyceryl trinitrate;

1 tablet contains 0.5 mg of nitroglycerin;

Excipients: lactose monohydrate; potato starch; sucrose; crospovidone; magnesium stearate.

Pharmaceutical form.

Sublingual tablets.

Main physicochemical properties: tablets are white or white with a yellowish tint, with a flat surface. The tablet surface may be rough.

Pharmacotherapeutic group.

Vasodilators used in cardiology. Organic nitrates. ATC code C01DA02.

Pharmacological properties.

Pharmacodynamics.

Nitroglycerin acts directly on smooth muscles, predominantly of venous and arterial vessels, via the nitrate receptor located in the smooth muscle layer of the vessel wall. Nitroglycerin is enzymatically converted within smooth muscle cells to produce nitric oxide (NO), which stimulates guanylate cyclase activity. This enzyme is responsible for 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 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 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, along with accumulation of cyclic adenosine monophosphate (cAMP) in the myocardium, enhances myocardial 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 decreasing preload, while arterial dilation reduces total peripheral resistance and afterload. Ultimately, this alleviates cardiac workload and improves coronary circulation.

There is a redistribution of myocardial blood flow 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 contributes to decreased energy expenditure by the left ventricle and reduced myocardial oxygen demand. Pulmonary capillary pressure decreases, allowing the use of nitroglycerin in myocardial infarction complicated by pulmonary edema and in heart failure. In cases of ischemic hypokinesia of certain myocardial segments, contractile function is restored.

Meningeal vessels dilate, while vessels of internal organs constrict. Pulmonary artery pressure decreases due to the vasodilatory and systemic effects of nitroglycerin. Nitroglycerin relaxes smooth muscles of the bronchi, biliary tract, gastrointestinal tract, and urinary tract. Experimental studies have not revealed teratogenic or embryotoxic effects.

Pharmacokinetics.

After sublingual administration, the effect develops within 0.5–2 minutes; 75% of patients report improvement within 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, decreases by 50% within 8 minutes, and nitroglycerin is almost 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 removed sequentially, both through the formation of inorganic nitrites and nitrates. The organic portion of nitrate ester molecules is converted into alcohols, aldehydes, and organic acids. Four hours after administration, nitrate esters (the initial compound) are almost 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 independent of 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 dinitrates, 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. 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. The elimination half-life of metabolites is 4 hours.

Clinical characteristics.

Indications.

Relief and short-term prophylaxis of angina attacks.

Contraindications.

Hypersensitivity to nitrates and excipients of the medicinal product; cerebral ischemia, 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, concomitant use of phosphodiesterase-5 (PDE-5) inhibitors (sildenafil, tadalafil, vardenafil), increased intracranial pressure, cardiac tamponade, angle-closure glaucoma with high intraocular pressure, toxic pulmonary edema, intracranial hemorrhage, recent head trauma, hemorrhagic stroke, aortic stenosis, conditions associated with reduced left ventricular filling pressure (acute myocardial infarction, isolated mitral stenosis, constrictive pericarditis).

Interaction with other medicinal products and other types of interactions.

When used concomitantly with other vasodilators, antihypertensive agents, angiotensin-converting enzyme inhibitors, calcium channel blockers ("slow" calcium channel blockers), phosphodiesterase inhibitors, diuretics, tricyclic antidepressants, monoamine oxidase inhibitors, ethanol and ethanol-containing preparations, β-adrenoblockers, procainamides, 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.

Atropine and other drugs exhibiting 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).

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

Phenobarbital activates nitrate metabolism in the liver. α-adrenomimetics, histamine, pituitrin, corticosteroids, central nervous system stimulants, bee and snake venom, and excessive sun exposure 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.

The drug should be prescribed with caution, carefully weighing the risks against the benefits, in the following conditions: uncontrolled hypovolemia; in patients with heart failure who have normal or low pulmonary artery pressure; severe anemia; hyperthyroidism; cerebrovascular disorders; severe renal and/or hepatic insufficiency (risk of methemoglobinemia development).

Use with caution in patients with marked cerebral atherosclerosis and in elderly patients. During treatment, alcohol consumption is prohibited; visits to saunas, baths, and hot showers are contraindicated.

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

With frequent use, tolerance (tolerance development) may occur to nitroglycerin, as with other organic nitrates, requiring dose escalation. To prevent tolerance during prolonged use of NITROGLYCERIN, an intermittent dosing regimen throughout the day (with a 10–12 hour nitrate-free interval) is recommended, or concomitant use of calcium antagonists, angiotensin-converting enzyme inhibitors, or diuretics. If tolerance develops, nitroglycerin may need to be temporarily discontinued (for several days) and replaced with antianginal agents from other pharmacotherapeutic groups.

Patients must inform their physician about any previous reactions to drugs in this class.

Significant hypotension and dizziness may occur upon nitroglycerin administration, especially when rapidly changing from a lying or sitting to a standing position, when consuming alcohol, or during physical exertion in hot weather.

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

Headache intensity associated with drug intake may be reduced by lowering the dose and/or co-administering valerodil.

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

Consult a physician before first-time use of the drug!

If you have known sugar intolerances, consult your physician before taking this medication.

Contains 0.005 g of sucrose per dose. Use with caution in patients with diabetes mellitus.

Contains 0.0289 g of lactose per dose. Use with caution in patients with diabetes mellitus.

This medicinal product is contraindicated in patients with rare hereditary conditions such as galactose intolerance, lactase deficiency, or glucose-galactose malabsorption syndrome.

Use during pregnancy or breastfeeding.

Nitroglycerin use during pregnancy or breastfeeding is contraindicated.

Effect on the ability to drive or operate machinery.

Nitroglycerin may impair reaction speed. Caution is advised when driving or operating machinery, which require high concentration.

Administration and Dosage

For use in adults.

When prescribing the drug for the first time, its effect on blood pressure levels should be evaluated. Monitoring the efficacy of nitroglycerin use must be performed by assessing heart rate and blood pressure levels.

For angina attacks, nitroglycerin should be administered sublingually immediately after the onset of symptoms. The usual dose is 1 tablet. A lower dose may be effective for many patients with stable angina. Therefore, if pain subsides quickly, the remaining portion of the tablet that has not completely dissolved should be spat out. If there is no antianginal effect within the first 5 minutes, another tablet should be taken.

If there is no therapeutic effect after taking 2–3 tablets, a doctor must be called immediately (possible myocardial infarction)!

Nitroglycerin acts for 30 minutes. In cases of frequent angina attacks, prolonged-release nitroglycerin preparations are recommended. However, if an angina attack occurs during treatment with prolonged-release nitrates, nitroglycerin should be used to relieve the acute attack. Tolerance to sublingual nitroglycerin develops rarely; however, if it occurs, the dose may need to be gradually increased in some patients, up to 2–3 tablets.

Children

There is no experience with the use of this drug in children; therefore, its use is not recommended in this age group.

Overdose

Symptoms: decreased blood pressure (below 90 mm Hg) with orthostatic dysregulation, headache, severe dizziness, loss of consciousness, rapid heartbeat, 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 legs elevated. In severe cases, administer plasma substitutes, sympathomimetics, oxygen; in cases of methemoglobinemia, administer methylene blue.

Adverse reactions.

Central nervous system: blurred vision, "nitrate" headache (especially at the beginning of treatment, decreases with prolonged therapy), dizziness and feeling of weakness, anxiety, psychotic reactions, drowsiness, disorientation.

Cardiovascular system: arterial hypotension, reflex tachycardia, rarely (especially in overdose) – orthostatic collapse, cyanosis, methemoglobinemia, facial flushing.

Gastrointestinal tract: possible nausea, vomiting, dry mouth, abdominal pain.

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

Other: restlessness, visual disturbances, exacerbation of glaucoma, hypothermia, sensation of warmth, respiratory disturbances, weakness.

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

Sometimes, with a sudden drop in arterial pressure, worsening of angina symptoms may occur (paradoxical "nitrate" reactions).

Shelf life.

2 years.

Storage conditions.

Store at a temperature not exceeding 30 °C in the original packaging, away from fire.

Keep out of reach of children.

Packaging.

40 tablets in bottles labeled in Ukrainian.

Or 40 tablets in polymer or glass bottles, 3 bottles in a blister with or without foil, 1 blister in a cardboard pack labeled in Ukrainian.

Or 25 tablets in polymer or glass bottles, 3 bottles in a blister with or without foil, 1 blister in a cardboard pack labeled in Ukrainian.

Prescription status.

Over-the-counter.

Manufacturer.

LLC NPF "MIKROKHIM" (responsible for batch release, excluding batch control/testing).

Manufacturer's address and place of business.

5, Budynstustriyi St., Kyiv, 01013, Ukraine.

To report an adverse event during the use of the medicinal product, please call +38 (050) 309-83-54 (24/7).

INSTRUCTION

for medical use of the medicinal product

NITROGLYCERIN

(NITROGLYCERIN)

Composition:

Active substance: glyceryl trinitrate;

1 tablet contains 0.5 mg of nitroglycerin;

Excipients: lactose monohydrate; potato starch; sucrose; crospovidone; magnesium stearate.

Pharmaceutical form.

Sublingual tablets.

Main physicochemical properties: white or white with a yellowish tint tablets, with a flat surface. The tablet surface may be rough.

Pharmacotherapeutic group.

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

Pharmacological properties.

Pharmacodynamics.

Nitroglycerin acts directly on smooth muscles, predominantly of venous and arterial vessels, via the nitrate receptor located in the smooth muscle layer of the vessel wall. Nitroglycerin is enzymatically converted within smooth muscle cells to produce nitric oxide (NO), which stimulates guanylate cyclase activity. This enzyme is responsible for the formation of cyclic guanosine-3',5'-monophosphate (cGMP), a 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 processes. Suppression of vasoconstrictive 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 parameters of the respiratory chain—the ratio of oxidized and 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 alleviates cardiac workload and improves coronary circulation.

Redistribution of myocardial blood flow occurs in favor of ischemic areas, and myocardial inotropic function is enhanced. End-diastolic pressure in the left ventricle and cardiac size are reduced, thereby improving blood supply to the subendocardial region of the myocardium, which is most vulnerable to ischemia. Reduced peripheral venous and arterial resistance and decreased cardiac filling pressure contribute to decreased energy expenditure by the left ventricle and reduced myocardial oxygen demand. Pulmonary capillary pressure decreases, allowing the use of nitroglycerin in myocardial infarction complicated by pulmonary edema and in heart failure. In cases of ischemic hypokinesis of certain myocardial segments, contractile function is restored.

Meningeal vessels dilate, while vessels of internal organs constrict. Pulmonary artery pressure decreases due to the vasodilatory and systemic effects of nitroglycerin. Nitroglycerin relaxes smooth muscles of the bronchi, bile ducts, gastrointestinal tract, and urinary tract. Experimental studies have not revealed teratogenic or toxic effects on the embryo.

Pharmacokinetics.

When administered sublingually, the effect develops within 0.5–2 minutes; 75% of patients report symptom improvement within 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. The concentration decreases by 50% within 8 minutes and nitroglycerin becomes almost 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 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. The organic portion of nitrate ester molecules is converted into alcohols, aldehydes, and organic acids. Nitrate esters (the initial compound) are almost undetectable 4 hours after administration. 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 independent of 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 dinitrates and mononitrates 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. The elimination half-life of metabolites is 4 hours.

Clinical characteristics.

Indications.

Relief and short-term prophylaxis of angina pectoris attacks.

Contraindications.

Hypersensitivity to nitrates and excipients of the medicinal product; cerebral ischemia, 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, concomitant use of phosphodiesterase-5 (PDE-5) inhibitors (sildenafil, tadalafil, vardenafil), increased intracranial pressure, cardiac tamponade, closed-angle glaucoma with high intraocular pressure, toxic pulmonary edema, intracranial hemorrhage, recent head trauma, hemorrhagic stroke, aortic stenosis, conditions associated with reduced left ventricular filling pressure (acute myocardial infarction, isolated mitral stenosis, constrictive pericarditis).

Interaction with other medicinal products and other types of interactions.

When used concomitantly with other vasodilators, antihypertensive agents, angiotensin-converting enzyme inhibitors, calcium channel blockers ("slow" calcium channel blockers), phosphodiesterase inhibitors (see section "Contraindications"), diuretics, tricyclic antidepressants, monoamine oxidase inhibitors, ethanol and ethanol-containing preparations, β-adrenoblockers, procainamides, 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.

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).

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

Phenobarbital enhances nitrate metabolism in the liver. α-adrenomimetics, histamine, pituitrin, corticosteroids, central nervous system stimulants, bee and snake venom, and excessive sun exposure 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 for use.

The medicinal product should be prescribed with caution, carefully weighing the risks and benefits, in the following conditions: uncontrolled hypovolemia; in patients with heart failure and normal or low pulmonary artery pressure; severe anemia; hyperthyroidism; cerebrovascular disorders; severe renal and/or hepatic impairment (risk of methemoglobinemia development).

Use with caution in patients with marked cerebral atherosclerosis and in elderly patients. During treatment, alcohol consumption is prohibited; visits to saunas, baths, and hot showers are contraindicated.

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

With frequent use, tolerance (tolerance development) may occur to nitroglycerin, as with other organic nitrates, requiring dose escalation. To prevent tolerance development during prolonged use of NITROGLYCERIN, intermittent dosing throughout the day (with 10–12 hour intervals) is recommended, or concomitant use of calcium antagonists, angiotensin-converting enzyme 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.

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

When taking nitroglycerin, a significant drop in arterial pressure and dizziness may occur when rapidly changing from a lying or sitting position to a standing position, during alcohol consumption, or during physical exertion in hot weather.

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

Headache intensity during drug administration may be reduced by lowering the dose and/or taking valerian or valerian-containing preparations (e.g., valeridol) simultaneously.

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 impairment. 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.

Before first use of the medicinal product, consult a physician!

If you have known sugar intolerances, consult your physician before taking this medicinal product.

Contains 0.005 g of sucrose per dose. Use with caution in patients with diabetes mellitus.

Contains 0.0289 g of lactose per dose. Use with caution in patients with diabetes mellitus.

The medicinal product is contraindicated in patients with rare hereditary conditions such as galactose intolerance, lactase deficiency, or glucose-galactose malabsorption syndrome.

Use during pregnancy or breastfeeding.

Nitroglycerin use during pregnancy or breastfeeding is contraindicated.

Ability to affect reaction speed when driving or operating machinery.

When driving vehicles or operating machinery requiring high concentration, nitroglycerin use may reduce reaction speed.

Method of Administration and Dosage

For use in adults.

When prescribing the drug for the first time, its effect on arterial blood pressure should be monitored. Efficacy of nitroglycerin use should be assessed by heart rate and arterial blood pressure.

For angina attacks, nitroglycerin should be administered sublingually immediately after the onset of symptoms. The usual dose is 1 tablet. A lower dose may be effective for many patients with stable angina. Therefore, if pain subsides quickly, the remaining part of the tablet that has not completely dissolved should be spat out. If no antianginal effect occurs within the first 5 minutes, another tablet should be taken.

If there is no therapeutic effect after taking 2–3 tablets, a doctor must be called immediately (possible myocardial infarction)!

Nitroglycerin remains effective for 30 minutes. In cases of frequent angina attacks, prolonged-release nitroglycerin preparations are recommended. However, if an angina attack occurs during treatment with prolonged-release nitrates, nitroglycerin should be used to relieve the acute episode. Tolerance to sublingual nitroglycerin rarely develops; however, if it occurs, in some patients the dose may need to be gradually increased up to 2–3 tablets.

Children

There is no experience with the use of this drug in children; 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, loss of consciousness, rapid heartbeat, nausea and vomiting, shortness of breath, marked 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 legs elevated. In severe cases, administer plasma substitutes, sympathomimetics, and oxygen. In cases of methemoglobinemia, administer methylene blue.

Adverse Reactions.

Central nervous system: blurred vision, "nitrate" headache (especially at the beginning of treatment; decreases with prolonged therapy), dizziness and feeling of weakness, anxiety, psychotic reactions, drowsiness, disorientation.

Cardiovascular system: arterial hypotension, reflex tachycardia, rarely (especially in cases of overdose) – orthostatic collapse, cyanosis, methemoglobinemia, facial flushing.

Gastrointestinal tract: possible nausea, vomiting, dry mouth, abdominal pain.

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

Other: restlessness, visual disturbances, exacerbation of glaucoma, hypothermia, sensation of warmth, respiratory disturbances, weakness.

There have also been isolated reports of adverse reactions: exacerbation of ischemic heart disease due to hypoxia, complete heart block, asystole, angioneurotic edema.

Sometimes, with a sudden drop in arterial pressure, an aggravation of angina symptoms may occur (paradoxical "nitrate" reactions).

Shelf life.

2 years.

Storage conditions.

Store at a temperature not exceeding 30 °C in the original packaging, away from fire.

Keep out of reach of children.

Packaging.

40 tablets in bottles labeled in Ukrainian.

Or 40 tablets in polymer or glass bottles, 3 bottles in a blister with or without foil, 1 blister per cardboard box labeled in Ukrainian.

Or 25 tablets in polymer or glass bottles, 3 bottles in a blister with or without foil, 1 blister per cardboard box labeled in Ukrainian.

Prescription status.

Over-the-counter.

Manufacturer.

LLC NPF "MIKROKHEM" (production unit (all stages of the manufacturing process)).

Manufacturer's address and location of business activity.

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

To report an adverse event during the use of this medicinal product, please call +38 (050) 309-83-54 (24/7).