Deproteynyzyrovann y hemoderyvat blood of lambs | Actovegin tablets 50 pcs.
Special Price
$42.68
Regular Price
$51.00
In stock
SKU
BID480871
Latin name
ACTOVEGIN
ACTOVEGIN
Latin name
ACTOVEGIN
Release form
Tablets, coated with a greenish-yellow color, round, biconvex, shiny.
Packing
50 pcs - dark glass bottles (1) - packs of cardboard.
Pharmacological action of
Enam® refers to drugs that affect the renin-angiotensin-aldosterone system (RAAS),
- ACE inhibitors. Enam® is used to treat essential hypertension (primary arterial hypertension (AH)) of any severity and renovascular hypertension both in monotherapy and in combination with other antihypertensive drugs, in particular with diuretics. Enam® is also used to treat or prevent the development of heart failure (HF).
Pharmacodynamics
Enam® is a derivative of two amino acids, L-alanine and L-proline.
After oral administration, enalapril is rapidly absorbed and hydrolyzed to enalaprilat, which is a highly specific and long-acting ACE inhibitor that does not contain a sulfhydryl group.
ACE (peptidyl dipeptidase A) catalyzes the conversion of angiotensin I to the pressor peptide angiotensin II.
After absorption, enalapril is hydrolyzed to enalaprilat, which inhibits ACE.
Inhibition of ACE leads to a decrease in the concentration of angiotensin II in blood plasma, which entails an increase in plasma renin activity (due to the elimination of negative feedback in response to renin release) and a decrease in aldosterone secretion.
ACE is identical to the kininase II enzyme, so enalapril can also block the destruction of bradykinin, a peptide with a pronounced vasodilating effect.
The significance of this effect in the therapeutic effect of enalapril needs to be clarified.
Despite the fact that the main mechanism by which enalapril lowers blood pressure (BP) is considered to be the suppression of RAAS activity, which plays an important role in the regulation of blood pressure, enalapril has an antihypertensive effect even in patients with hypertension and with a reduced plasma renin activity.
The use of enalapril in patients with hypertension leads to a decrease in blood pressure both in the standing position and in the lying position without a significant increase in heart rate (HR).
Symptomatic postural hypotension develops infrequently.
In some patients, achieving optimal BP reduction may require several weeks of therapy.
Interruption of enalapril therapy does not cause a sharp rise in blood pressure.
Effective inhibition of ACE activity usually develops 2-4 hours after a single oral dose of enalapril. An antihypertensive effect develops within 1 hour, the maximum decrease in blood pressure is observed 4-6 hours after taking the drug. The duration of action depends on the dose.
However, when using the recommended doses, the antihypertensive effect and hemodynamic effects persist for 24 hours.
Antihypertensive therapy with enalapril leads to a significant regression of left ventricular hypertrophy and the preservation of its systolic function.
In clinical studies of hemodynamics in patients with essential hypertension, a decrease in blood pressure was accompanied by a decrease in total peripheral vascular resistance, an increase in cardiac output, and no changes or slight changes in heart rate. After taking enalapril, an increase in renal blood flow was observed.
In this case, the glomerular filtration rate (GFR) did not change, there were no signs of sodium or fluid retention.
However, in patients with initially reduced glomerular filtration, its rate usually increased.
Long-term use of enalapril in patients with essential hypertension and renal failure may lead to an improvement in renal function, as evidenced by an increase in GFR.
In short clinical trials, in patients with renal failure and with or without diabetes mellitus,
after taking enalapril showed a decrease in albuminuria, kidney excretion of IgG, and a decrease in total protein in the urine.
With the simultaneous use of enalapril and thiazide diuretics, a more pronounced antihypertensive effect is observed.
Enalapril reduces or prevents the development of hypokalemia caused by thiazide administration.
Enalapril therapy is usually not associated with an undesirable effect on the concentration of uric acid in blood plasma.
Enalapril therapy is accompanied by a beneficial effect on the ratio of plasma lipoprotein fractions and a lack of effect or a beneficial effect on the concentration of total cholesterol.
In patients with heart failure, on the background of therapy with cardiac glycosides and diuretics, enalapril caused a decrease in total peripheral resistance and blood pressure. Cardiac output increased, while heart rate (usually increased in patients with heart failure) decreased.
The jamming pressure in the pulmonary capillaries also decreased.
Exercise tolerance and severity of HF, assessed according to the criteria of the New York Heart Association (NYHA), improved. These effects were observed with prolonged therapy.
In patients with mild to moderate severity of heart failure, enalapril slowed the progression of heart dilatation and heart failure, as evidenced by a decrease in the final diastolic and systolic volumes of the left ventricle and an improvement in the ejection fraction of the left ventricle.
Clinical data have shown that enalapril reduces the frequency of ventricular arrhythmias in patients with heart failure, although the underlying mechanisms and clinical significance of this effect are not known.
Pharmacokinetics
Absorption
After oral administration, enalapril is rapidly absorbed in the gastrointestinal tract.
The maximum concentration of enalapril in serum is reached within 1 hour after oral administration.
Enalapril absorption by ingestion is approximately 60%.
Eating does not affect the absorption of enalapril.
After absorption, enalapril is rapidly hydrolyzed to form the active metabolite of enalaprilat, a potent ACE inhibitor.
The maximum concentration of enalaprilat in serum is observed approximately 4 hours after ingestion of a dose of enalapril. The duration of absorption and hydrolysis of enalapril is similar for the various recommended therapeutic doses.
In healthy volunteers with normal renal function, the equilibrium concentration of enalaprilat in serum is reached by the 4th day from the start of enalapril administration.
Distribution of
In the therapeutic dose range, the binding of enalaprilat to plasma proteins does not exceed 60%.
Metabolism
There are no data on other significant metabolic pathways of enalapril, other than hydrolysis to enalaprilat.
Excretion
Enalapril is excreted primarily through the kidneys.
The main metabolites detected in the urine are enalaprilat, approximately 40% of the dose, and unchanged enalapril (about 20%).
The plasma concentration curve of enalaprilate has a long final phase,
apparently due to its binding to ACE.
The half-life of enalaprilat when administered internally is 11 hours.
Pharmacokinetics in special patient groups
Patients with impaired renal function
The area under the concentration-time (AUC) curve of enalapril and enalaprilat increases in patients with renal failure.
\ In patients with mild to moderate severity of renal failure (creatinine clearance
(CC) 40-60 ml / min), after taking enalapril at a dose of 5 mg 1 time per day, the equilibrium AUC of enalaprilat was approximately 2 times higher. than in patients with unchanged renal function. increases energy metabolism and glucose intake.
As a result, the energy resources of the cell increase, especially in conditions of lack of energy. The Actovegin inositol phosphate oligosaccharide fraction activates pyruvate dehydrogenase (PDH), which leads to an increase in glucose utilization. An increase in oxygen consumption under the influence of Actovegin leads to stabilization of the plasma membranes of cells during ischemia and reduces the formation of lactates.
Actovegin not only increases intracellular glucose, but also improves oxidative metabolism, thereby improving the energy supply of the cell, as evidenced by an increase in the concentration of direct free energy carriers such as ATP, ADP, phosphocreatine, as well as amino acids, for example glutamate, aspartate and GABA . In cases of metabolic and cerebral blood flow disorders, for example, with cerebral insufficiency syndrome (dementia), glucose transport through the BBB and its utilization by cells deteriorate.
PDH activity and acetylcholine concentration are also reduced. The use of Actovegin helps to normalize these indicators, improves transport and utilization of glucose, while there is an increase in oxygen consumption.
Actovegin has been shown to act in the same way with peripheral (arterial, venous) circulatory disorders and the corresponding consequences of such disorders (arterial angiopathy, ulcerative lesions of the lower extremities), as well as when used to accelerate wound healing.
For ulcers of various etiologies, trophic disorders (bedsores), burns and radiation injuries Actovegin improves not only morphological, but also biochemical parameters of granulation, for example, increases the concentration of DNA, hemoglobin and hydroxyproline. The effect of Actovegin begins to appear no later than 30 minutes (10-30 minutes) after ingestion and reaches a maximum on average after 3 hours (2-6 hours).
Indications of
as part of the complex therapy of metabolic and vascular disorders of the brain (various forms of cerebrovascular insufficiency, dementia, traumatic brain injury)
peripheral (arterial and venous) vascular disorders and their consequences (angiopathy, trophic ulcer disease) srd.
Contraindications
hypersensitivity to the components of the drug or to similar drugs.
With caution, the drug should be prescribed for heart failure stage II-III, pulmonary edema, oliguria, anuria, hyperhydration, during pregnancy and lactation.
Use during pregnancy and lactation
Use of ActoveginВ® during pregnancy and lactation is allowed, but caution should be exercised.
Composition
1 tab.
deproteinized calf hemoderivative 200 mg
Excipients:
magnesium stearate - 2.0 mg,
povidone K90 - 10.0 mg,
talcum powder - 3.0 mg,
microcrystalline cellulose - 135.0 mg.
Shell composition:
acacia gum - 6.8 mg,
mountain glycol wax - 0.1 mg,
hypromellose phthalate - 29.45 mg,
diethyl phthalate - 11.8 mg,
dye quinoline yellow aluminum varnish - 2.0 mg, srdlk 2.95 mg, srdlk 2. povidone K30 - 1.54 mg,
sucrose - 52.3 mg,
talcum - 42.2 mg,
titanium dioxide - 0.86 mg.
Dosage and administration
Doses and route of administration depend on the indications and severity of the disease.
Inside appoint 1-2 tablets 3 times / day before meals. The tablet is not chewed, washed down with a small amount of water.
Duration of treatment is 4-6 weeks.
Side effects
Allergic reactions: rarely (with a history of hypersensitivity reactions) - urticaria, swelling, flushing, increased sweating, increased body temperature, shock.
Drug Interaction
Drug Interaction Actovegin has not been established.
Overdose
Symptoms: undesirable effects from the digestive system. Treatment: carrying out symptomatic therapy.
Storage conditions
The drug should be stored out of the reach of children, protected from light at a temperature not exceeding 25 РC.
Expiration
Expiration is 3 years. Do not use after the expiry date.
Deystvuyuschee substances
Deproteynyzyrovann y hemoderyvat blood of lambs
drugstore terms and conditions prescription
Dosage form srdl kp Dosage form
tablets
Takeda GmbH, Russia
ACTOVEGIN
Release form
Tablets, coated with a greenish-yellow color, round, biconvex, shiny.
Packing
50 pcs - dark glass bottles (1) - packs of cardboard.
Pharmacological action of
Enam® refers to drugs that affect the renin-angiotensin-aldosterone system (RAAS),
- ACE inhibitors. Enam® is used to treat essential hypertension (primary arterial hypertension (AH)) of any severity and renovascular hypertension both in monotherapy and in combination with other antihypertensive drugs, in particular with diuretics. Enam® is also used to treat or prevent the development of heart failure (HF).
Pharmacodynamics
Enam® is a derivative of two amino acids, L-alanine and L-proline.
After oral administration, enalapril is rapidly absorbed and hydrolyzed to enalaprilat, which is a highly specific and long-acting ACE inhibitor that does not contain a sulfhydryl group.
ACE (peptidyl dipeptidase A) catalyzes the conversion of angiotensin I to the pressor peptide angiotensin II.
After absorption, enalapril is hydrolyzed to enalaprilat, which inhibits ACE.
Inhibition of ACE leads to a decrease in the concentration of angiotensin II in blood plasma, which entails an increase in plasma renin activity (due to the elimination of negative feedback in response to renin release) and a decrease in aldosterone secretion.
ACE is identical to the kininase II enzyme, so enalapril can also block the destruction of bradykinin, a peptide with a pronounced vasodilating effect.
The significance of this effect in the therapeutic effect of enalapril needs to be clarified.
Despite the fact that the main mechanism by which enalapril lowers blood pressure (BP) is considered to be the suppression of RAAS activity, which plays an important role in the regulation of blood pressure, enalapril has an antihypertensive effect even in patients with hypertension and with a reduced plasma renin activity.
The use of enalapril in patients with hypertension leads to a decrease in blood pressure both in the standing position and in the lying position without a significant increase in heart rate (HR).
Symptomatic postural hypotension develops infrequently.
In some patients, achieving optimal BP reduction may require several weeks of therapy.
Interruption of enalapril therapy does not cause a sharp rise in blood pressure.
Effective inhibition of ACE activity usually develops 2-4 hours after a single oral dose of enalapril. An antihypertensive effect develops within 1 hour, the maximum decrease in blood pressure is observed 4-6 hours after taking the drug. The duration of action depends on the dose.
However, when using the recommended doses, the antihypertensive effect and hemodynamic effects persist for 24 hours.
Antihypertensive therapy with enalapril leads to a significant regression of left ventricular hypertrophy and the preservation of its systolic function.
In clinical studies of hemodynamics in patients with essential hypertension, a decrease in blood pressure was accompanied by a decrease in total peripheral vascular resistance, an increase in cardiac output, and no changes or slight changes in heart rate. After taking enalapril, an increase in renal blood flow was observed.
In this case, the glomerular filtration rate (GFR) did not change, there were no signs of sodium or fluid retention.
However, in patients with initially reduced glomerular filtration, its rate usually increased.
Long-term use of enalapril in patients with essential hypertension and renal failure may lead to an improvement in renal function, as evidenced by an increase in GFR.
In short clinical trials, in patients with renal failure and with or without diabetes mellitus,
after taking enalapril showed a decrease in albuminuria, kidney excretion of IgG, and a decrease in total protein in the urine.
With the simultaneous use of enalapril and thiazide diuretics, a more pronounced antihypertensive effect is observed.
Enalapril reduces or prevents the development of hypokalemia caused by thiazide administration.
Enalapril therapy is usually not associated with an undesirable effect on the concentration of uric acid in blood plasma.
Enalapril therapy is accompanied by a beneficial effect on the ratio of plasma lipoprotein fractions and a lack of effect or a beneficial effect on the concentration of total cholesterol.
In patients with heart failure, on the background of therapy with cardiac glycosides and diuretics, enalapril caused a decrease in total peripheral resistance and blood pressure. Cardiac output increased, while heart rate (usually increased in patients with heart failure) decreased.
The jamming pressure in the pulmonary capillaries also decreased.
Exercise tolerance and severity of HF, assessed according to the criteria of the New York Heart Association (NYHA), improved. These effects were observed with prolonged therapy.
In patients with mild to moderate severity of heart failure, enalapril slowed the progression of heart dilatation and heart failure, as evidenced by a decrease in the final diastolic and systolic volumes of the left ventricle and an improvement in the ejection fraction of the left ventricle.
Clinical data have shown that enalapril reduces the frequency of ventricular arrhythmias in patients with heart failure, although the underlying mechanisms and clinical significance of this effect are not known.
Pharmacokinetics
Absorption
After oral administration, enalapril is rapidly absorbed in the gastrointestinal tract.
The maximum concentration of enalapril in serum is reached within 1 hour after oral administration.
Enalapril absorption by ingestion is approximately 60%.
Eating does not affect the absorption of enalapril.
After absorption, enalapril is rapidly hydrolyzed to form the active metabolite of enalaprilat, a potent ACE inhibitor.
The maximum concentration of enalaprilat in serum is observed approximately 4 hours after ingestion of a dose of enalapril. The duration of absorption and hydrolysis of enalapril is similar for the various recommended therapeutic doses.
In healthy volunteers with normal renal function, the equilibrium concentration of enalaprilat in serum is reached by the 4th day from the start of enalapril administration.
Distribution of
In the therapeutic dose range, the binding of enalaprilat to plasma proteins does not exceed 60%.
Metabolism
There are no data on other significant metabolic pathways of enalapril, other than hydrolysis to enalaprilat.
Excretion
Enalapril is excreted primarily through the kidneys.
The main metabolites detected in the urine are enalaprilat, approximately 40% of the dose, and unchanged enalapril (about 20%).
The plasma concentration curve of enalaprilate has a long final phase,
apparently due to its binding to ACE.
The half-life of enalaprilat when administered internally is 11 hours.
Pharmacokinetics in special patient groups
Patients with impaired renal function
The area under the concentration-time (AUC) curve of enalapril and enalaprilat increases in patients with renal failure.
\ In patients with mild to moderate severity of renal failure (creatinine clearance
(CC) 40-60 ml / min), after taking enalapril at a dose of 5 mg 1 time per day, the equilibrium AUC of enalaprilat was approximately 2 times higher. than in patients with unchanged renal function. increases energy metabolism and glucose intake.
As a result, the energy resources of the cell increase, especially in conditions of lack of energy. The Actovegin inositol phosphate oligosaccharide fraction activates pyruvate dehydrogenase (PDH), which leads to an increase in glucose utilization. An increase in oxygen consumption under the influence of Actovegin leads to stabilization of the plasma membranes of cells during ischemia and reduces the formation of lactates.
Actovegin not only increases intracellular glucose, but also improves oxidative metabolism, thereby improving the energy supply of the cell, as evidenced by an increase in the concentration of direct free energy carriers such as ATP, ADP, phosphocreatine, as well as amino acids, for example glutamate, aspartate and GABA . In cases of metabolic and cerebral blood flow disorders, for example, with cerebral insufficiency syndrome (dementia), glucose transport through the BBB and its utilization by cells deteriorate.
PDH activity and acetylcholine concentration are also reduced. The use of Actovegin helps to normalize these indicators, improves transport and utilization of glucose, while there is an increase in oxygen consumption.
Actovegin has been shown to act in the same way with peripheral (arterial, venous) circulatory disorders and the corresponding consequences of such disorders (arterial angiopathy, ulcerative lesions of the lower extremities), as well as when used to accelerate wound healing.
For ulcers of various etiologies, trophic disorders (bedsores), burns and radiation injuries Actovegin improves not only morphological, but also biochemical parameters of granulation, for example, increases the concentration of DNA, hemoglobin and hydroxyproline. The effect of Actovegin begins to appear no later than 30 minutes (10-30 minutes) after ingestion and reaches a maximum on average after 3 hours (2-6 hours).
Indications of
as part of the complex therapy of metabolic and vascular disorders of the brain (various forms of cerebrovascular insufficiency, dementia, traumatic brain injury)
peripheral (arterial and venous) vascular disorders and their consequences (angiopathy, trophic ulcer disease) srd.
Contraindications
hypersensitivity to the components of the drug or to similar drugs.
With caution, the drug should be prescribed for heart failure stage II-III, pulmonary edema, oliguria, anuria, hyperhydration, during pregnancy and lactation.
Use during pregnancy and lactation
Use of ActoveginВ® during pregnancy and lactation is allowed, but caution should be exercised.
Composition
1 tab.
deproteinized calf hemoderivative 200 mg
Excipients:
magnesium stearate - 2.0 mg,
povidone K90 - 10.0 mg,
talcum powder - 3.0 mg,
microcrystalline cellulose - 135.0 mg.
Shell composition:
acacia gum - 6.8 mg,
mountain glycol wax - 0.1 mg,
hypromellose phthalate - 29.45 mg,
diethyl phthalate - 11.8 mg,
dye quinoline yellow aluminum varnish - 2.0 mg, srdlk 2.95 mg, srdlk 2. povidone K30 - 1.54 mg,
sucrose - 52.3 mg,
talcum - 42.2 mg,
titanium dioxide - 0.86 mg.
Dosage and administration
Doses and route of administration depend on the indications and severity of the disease.
Inside appoint 1-2 tablets 3 times / day before meals. The tablet is not chewed, washed down with a small amount of water.
Duration of treatment is 4-6 weeks.
Side effects
Allergic reactions: rarely (with a history of hypersensitivity reactions) - urticaria, swelling, flushing, increased sweating, increased body temperature, shock.
Drug Interaction
Drug Interaction Actovegin has not been established.
Overdose
Symptoms: undesirable effects from the digestive system. Treatment: carrying out symptomatic therapy.
Storage conditions
The drug should be stored out of the reach of children, protected from light at a temperature not exceeding 25 РC.
Expiration
Expiration is 3 years. Do not use after the expiry date.
Deystvuyuschee substances
Deproteynyzyrovann y hemoderyvat blood of lambs
drugstore terms and conditions prescription
Dosage form srdl kp Dosage form
tablets
Takeda GmbH, Russia
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