PROPRANOLOL HYDROCHLORIDE

Pharmacological properties of the drug Propranolol

Propranolol is a lipophilic non-selective β-adrenergic receptor blocker without BCA. Reduces the frequency and strength of heart contractions, slows down AV conduction, and reduces the myocardium's need for oxygen. It has a membrane-stabilizing effect and reduces the incidence of ectopic foci. The therapeutic effect consists of a negative chronotropic and inotropic effect on the myocardium. The hypotensive effect stabilizes by the end of 2 weeks of treatment. Propranolol is resorbed from the digestive tract by more than 90% and during the initial passage through the liver is metabolized by almost 70%. Bioavailability - about 30%. With long-term use, propranolol is almost completely metabolized, and up to 18 different metabolites can be identified. 4-Hydroxypropranolol has weak β-adrenolytic activity. The volume of distribution of propranolol is 3.61 l/kg, binding to plasma proteins is 93%. The maximum concentration in blood plasma is achieved 1–2 hours after administration. Elimination of propranolol occurs primarily through the liver and more than 90% in the form of metabolites. The half-life is 3–6 hours.

When used simultaneously with hypoglycemic agents, there is a risk of developing hypoglycemia due to the increased effect of hypoglycemic agents.

When used simultaneously with MAO inhibitors, there is a possibility of developing undesirable manifestations of drug interactions.

Cases of the development of severe bradycardia have been described when using propranolol for arrhythmia caused by digitalis drugs.

When used simultaneously with drugs for inhalation anesthesia, the risk of suppression of myocardial function and the development of arterial hypotension increases.

When used simultaneously with amiodarone, arterial hypotension, bradycardia, ventricular fibrillation, and asystole are possible.

When used simultaneously with verapamil, arterial hypotension, bradycardia, and dyspnea are possible. Cmax in the blood plasma increases, AUC increases, and the clearance of propranolol decreases due to inhibition of its metabolism in the liver under the influence of verapamil.

Propranolol does not affect the pharmacokinetics of verapamil.

A case of severe arterial hypotension and cardiac arrest has been described when used simultaneously with haloperidol.

When used simultaneously with hydralazine, the Cmax in the blood plasma and the AUC of propranolol increase. It is believed that hydralazine may reduce hepatic blood flow or inhibit the activity of liver enzymes, resulting in a slower metabolism of propranolol.

When used simultaneously, propranolol can inhibit the effects of glibenclamide, glyburide, chlorpropamide, tolbutamide, because Non-selective beta2-blockers are able to block pancreatic beta2-adrenergic receptors associated with insulin secretion.

The release of insulin from the pancreas due to the action of sulfonylurea derivatives is inhibited by beta-blockers, which to some extent prevents the development of the hypoglycemic effect.

When used simultaneously with diltiazem, the concentration of propranolol in the blood plasma increases due to inhibition of its metabolism under the influence of diltiazem. An additive depressant effect on cardiac function is observed due to the slowing of impulse conduction through the AV node caused by diltiazem. There is a risk of developing severe bradycardia, stroke and minute volume are significantly reduced.

With simultaneous use, cases of increased concentrations of warfarin and phenindione in the blood plasma have been described.

When used concomitantly with doxorubicin, experimental studies have shown increased cardiotoxicity.

When used simultaneously, propranolol prevents the development of the bronchodilator effect of isoprenaline, salbutamol, and terbutaline.

With simultaneous use, cases of increased concentrations of imipramine in the blood plasma have been described.

When used simultaneously with indomethacin, naproxen, piroxicam, acetylsalicylic acid, the antihypertensive effect of propranolol may be reduced.

When used simultaneously with ketanserin, an additive hypotensive effect may develop.

When used simultaneously with clonidine, the antihypertensive effect is enhanced.

In patients receiving propranolol, severe arterial hypertension may develop if clonidine is abruptly discontinued. It is believed that this is due to an increase in the content of catecholamines in the circulating blood and an increase in their vasoconstrictor effect.

When used simultaneously with caffeine, the effectiveness of propranolol may be reduced.

With simultaneous use, it is possible to enhance the effects of lidocaine and bupivacaine (including toxic ones), apparently due to a slowdown in the metabolism of local anesthetics in the liver.

When used simultaneously with lithium carbonate, a case of bradycardia has been described.

With simultaneous use, a case of increased side effects of maprotiline has been described, which is apparently due to a slowdown in its metabolism in the liver and accumulation in the body.

When used simultaneously with mefloquine, the QT interval increases, and a case of cardiac arrest has been described; with morphine - the inhibitory effect on the central nervous system caused by morphine is enhanced; with sodium amidotrizoate - cases of severe arterial hypotension have been described.

When used simultaneously with nisoldipine, an increase in the Cmax and AUC of propranolol and nisoldipine in the blood plasma is possible, which leads to severe arterial hypotension. There is a report of increased beta-blocking action.

Cases of increased Cmax and AUC of propranolol, arterial hypotension and a decrease in heart rate have been described when used simultaneously with nicardipine.

When used simultaneously with nifedipine in patients with coronary artery disease, severe arterial hypotension may develop, increasing the risk of heart failure and myocardial infarction, which may be due to an increase in the negative inotropic effect of nifedipine.

Patients receiving propranolol are at risk of developing severe hypotension after taking the first dose of prazosin.

When used simultaneously with prenylamine, the QT interval increases.

When used simultaneously with propafenone, the concentration of propranolol in the blood plasma increases and a toxic effect develops. Propafenone is believed to inhibit the hepatic metabolism of propranolol, reducing its clearance and increasing serum concentrations.

With the simultaneous use of reserpine and other antihypertensive drugs, the risk of developing arterial hypotension and bradycardia increases.

With simultaneous use, the Cmax and AUC of rizatriptan increases; with rifampicin - the concentration of propranolol in the blood plasma decreases; with suxamethonium chloride, tubocurarine chloride - the effect of muscle relaxants may change.

With simultaneous use, the clearance of theophylline decreases due to a slowdown in its metabolism in the liver. There is a risk of developing bronchospasm in patients with bronchial asthma or COPD. Beta blockers may block the inotropic effect of theophylline.

When used simultaneously with phenindione, cases of a slight increase in bleeding without changes in blood clotting parameters have been described.

When used concomitantly with flecainide, additive cardiodepressive effects are possible.

Fluoxetine inhibits the CYP2D6 isoenzyme, which leads to inhibition of the metabolism of propranolol and its accumulation and may enhance the cardiodepressive effect (including bradycardia). Fluoxetine and, mainly, its metabolites are characterized by a long T1/2, so the likelihood of drug interactions remains even several days after discontinuation of fluoxetine.

Quinidine inhibits the CYP2D6 isoenzyme, which leads to inhibition of the metabolism of propranolol, while its clearance decreases. Increased beta-blocking action and orthostatic hypotension are possible.

With simultaneous use in the blood plasma, the concentrations of propranolol, chlorpromazine, and thioridazine increase. A sharp decrease in blood pressure is possible.

Cimetidine inhibits the activity of microsomal liver enzymes (including the CYP2D6 isoenzyme), this leads to inhibition of the metabolism of propranolol and its cumulation: an increase in negative inotropic effect and the development of a cardiodepressive effect are observed.

With simultaneous use, the hypertensive effect of epinephrine is enhanced, and there is a risk of developing severe life-threatening hypertensive reactions and bradycardia. The bronchodilator effect of sympathomimetics (epinephrine, ephedrine) decreases.

With simultaneous use, cases of decreased effectiveness of ergotamine have been described.

There are reports of changes in the hemodynamic effects of propranolol when used simultaneously with ethanol.

Side effects of the drug Propranolol

Increased fatigue, dizziness, headache, paresthesia and feeling of coldness in the extremities, dyspepsia, bronchospasm, skin reactions, conjunctivitis, increasing signs of heart failure, bradycardia, AV conduction disorders, arterial hypotension, sleep disturbances, depression, nightmares, hallucinations, increased peripheral circulation disorders, decreased lacrimation, hypoglycemia, a feeling of dry mouth, muscle cramps and weakness, potency disorders, in some cases - blurred vision and keratoconjunctivitis, increased angina attacks.

Special instructions for the use of the drug Propranolol

Patients with pheochromocytoma should be given concurrent α-adrenergic blockers. Propranolol should be used with caution in cases of AV conduction disorders, in patients with diabetes mellitus and during fasting. In case of impaired liver and kidney function, it is necessary to reduce the dose of propranolol. Propranolol can affect the body's psychophysical abilities, weakening attention and slowing down responses, especially when consuming alcohol or taking drugs that depress the central nervous system. Propranolol penetrates the placental barrier. No studies have been conducted on the use of propranolol in the first trimester of pregnancy. In order to prevent bradycardia, arterial hypotension, hypoglycemia, respiratory depression (neonatal asphyxia) in a newborn, it is necessary to interrupt propranolol therapy 48–72 hours before the expected date of birth. The newborn should be left under medical supervision for 48–72 hours.

Propranolol

Monitoring of patients taking the drug should include monitoring heart rate and blood pressure (at the beginning of treatment - daily, then once every 3-4 months), ECG, blood glucose concentration in patients with diabetes (once every 4-5 months) . In elderly patients, it is recommended to monitor renal function (once every 4-5 months).

The patient should be taught how to calculate heart rate and instructed about the need for medical consultation if the heart rate is less than 50/min.

Before prescribing the drug to patients with CHF (early stages), it is necessary to use digitalis and/or diuretics.

In smokers, the effectiveness of beta-blockers is lower.

Patients using contact lenses should take into account that during treatment the production of tear fluid may decrease.

Patients with pheochromocytoma are prescribed only after taking an alpha-blocker.

In case of thyrotoxicosis, the drug can mask certain clinical signs of thyrotoxicosis (for example, tachycardia). Abrupt withdrawal in patients with thyrotoxicosis is contraindicated because it can increase symptoms.

When prescribing beta-blockers to patients receiving hypoglycemic drugs, caution should be exercised, since hypoglycemia may develop during long breaks in food intake. Moreover, its symptoms such as tachycardia or tremor will be masked due to the action of the drug. Patients should be instructed that the main symptom of hypoglycemia during treatment with beta-blockers is increased sweating.

When taking clonidine concomitantly, it can be discontinued only a few days after propranolol is discontinued.

It is possible that the severity of the hypersensitivity reaction may increase and the absence of effect from usual doses of epinephrine against the background of a burdened allergic history.

A few days before general anesthesia with chloroform or ether, you must stop taking the drug. If the patient took the drug before surgery, he should select a drug for general anesthesia with minimal negative inotropic effect.

Reciprocal activation of the n.vagus can be eliminated by intravenous administration of atropine (1-2 mg).

Drugs that reduce catecholamine reserves (for example, reserpine) can enhance the effect of beta-blockers, so patients taking such combinations of drugs should be under constant medical supervision to detect arterial hypotension or bradycardia.

Cannot be used simultaneously with antipsychotic drugs (neuroleptics) and anxiolytic drugs (tranquilizers).

Use with caution in combination with psychoactive drugs, such as MAO inhibitors, when taking them on a course for more than 2 weeks.

If elderly patients develop increasing bradycardia (less than 50/min), arterial hypotension (systolic blood pressure below 100 mm Hg), AV block, bronchospasm, ventricular arrhythmias, severe liver and kidney dysfunction, it is necessary to reduce the dose or stop treatment . It is recommended to discontinue therapy if depression caused by taking beta-blockers develops.

Treatment should not be abruptly interrupted due to the risk of developing severe arrhythmias and myocardial infarction. Cancellation is carried out gradually, reducing the dose over 2 weeks or more (by 25% in 3-4 days).

Use during pregnancy and lactation is possible if the benefit to the mother outweighs the risk of side effects in the fetus and child. If it is necessary to take it during pregnancy, carefully monitor the condition of the fetus; it should be discontinued 48-72 hours before birth.

Catecholamines, normetanephrine and vanillylmandelic acid should be discontinued before blood and urine tests; antinuclear antibody titers.

During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Drug interactions Propranolol

During IV therapy with calcium antagonists (verapamil and diltiazem), the use of β-adrenergic receptor blockers is contraindicated (except for intensive therapy). With the simultaneous administration of propranolol and norepinephrine or MAO inhibitors, a sharp increase in blood pressure is possible. When propranolol is combined with tricyclic antidepressants, barbiturates, anesthetics, antihypertensive and vasodilator drugs and diuretics, a sharp decrease in blood pressure is observed. The cardiodepressive effect of propranolol is potentiated by its combination with antiarrhythmic or anesthetic drugs. The negative chronotropic and dromotropic effect of propranolol is manifested when it is taken in combination with reserpine, clonidine, methyldopa, guanfacine and cardiac glycosides. Propranolol enhances the effects of tubocurarine. When taking propranolol and insulin or oral hypoglycemic drugs, the symptoms of hypoglycemia are masked, especially during physical activity. Cimetidine increases the content of propranolol in the blood plasma.

Propranolol

Abiraterone. It is recommended to prescribe abiraterone with caution to patients receiving propranolol (metabolized through the CYP2D6 system, has a narrow therapeutic index). In such cases, a reduction in the dose of propranolol should be considered.

Agomelatine. Caution should be exercised when administering agomelatine concomitantly with propranolol (a moderate inhibitor of the CYP1A2 isoenzyme) until sufficient clinical experience has been gained.

Amiodarone. When amiodarone is used concomitantly with propranolol, the risk of developing or worsening bradycardia, AV block, cardiac arrest and heart failure increases.

Amiodarone. With amiodarone (which has weak beta-blocking activity), the risk of excessive hypotension and bradycardia increases.

Articaine + Epinephrine. The simultaneous use of the combination of articaine + epinephrine with propranolol is contraindicated due to the risk of developing a hypertensive crisis and severe bradycardia.

Atracuria besilate. Propranolol, when used in combination with atracurium besylate, enhances neuromuscular blockade and can intensify or unmask latent myasthenia gravis or cause myasthenic syndrome, which can lead to the development of hypersensitivity to atracurium besylate.

Acetylsalicylic acid. Acetylsalicylic acid weakens the hypotensive effect of propranolol (a consequence of inhibition of PG synthesis in the kidneys with a decrease in renal blood flow and sodium and fluid retention).

Belladonna leaf extract + Benzocaine + Metamizole sodium + Sodium bicarbonate. The effect of the combination of belladonna leaf extract + benzocaine + metamizole sodium + sodium bicarbonate is enhanced by propranolol (slows down inactivation).

Belladonna leaf extract + Caffeine + Paracetamol + Theophylline + Phenobarbital + Cytisine + Ephedrine. Propranolol increases the concentration of theophylline (in the combination of belladonna leaf extract + caffeine + paracetamol + theophylline + phenobarbital + cytisine + ephedrine) in the blood and therefore may increase the risk of developing its side effects.

Bendazole + Metamizole sodium + Papaverine + Phenobarbital. Combination with propranolol enhances the hypotensive effect of the combination of bendazole + metamizole sodium + papaverine + phenobarbital.

Benzathine benzylpenicillin. It increases the content of the free fraction in plasma, since, having a greater ability to bind to proteins, it displaces it from the sites of fixation.

Betaxolol. Propranolol enhances (mutually) the effects. Beta-blockers prescribed orally, incl. propranolol, together with beta-blockers used in ophthalmology (eye drops), incl. betaxolol, enhance the reduction of IOP; in this case, the effects of systemic blockade of beta-adrenergic receptors, as a rule, increase.

Bisoprolol. Mutually enhances the effects; combined use is contraindicated.

Bromhexine + Guaifenesin + Salbutamol. It is not recommended to use the combination of bromhexine + guaifenesin + salbutamol simultaneously with propranolol.

Bromhexine + Guaifenesin + Salbutamol + Racementol. It is not recommended to use the combination of bromhexine + guaifenesin + salbutamol + racementol simultaneously with propranolol.

Bupivacaine + Epinephrine. When used in combination, propranolol, a non-cardioselective beta-blocker, enhances the pressor effect of epinephrine (as part of a combination of bupivacaine + epinephrine), which can lead to severe hypertension and bradycardia.

Warfarin. Propranolol, when used in combination, prolongs the anticoagulant effect of warfarin.

Warfarin. Propranolol increases the effect of warfarin.

Verapamil. Concomitant use of propranolol and intravenous administration of verapamil is contraindicated.

Verapamil. Propranolol enhances (mutually) the effect and can increase the negative effect on heart rate, AV conduction and/or cardiac contractility, causing severe bradycardia, AV block (up to complete). Against the background of verapamil, clearance decreases.

Hydralazine. The combined use of propranolol with hydralazine increases the risk of an excessive decrease in blood pressure.

Hydrochlorothiazide. Strengthens (mutually) the antihypertensive effect.

Hydrochlorothiazide + Captopril. The combination of hydrochlorothiazide + captopril increases the bioavailability of propranolol and enhances (mutually) the effects.

Glimepiride. Propranolol increases (by 20%) Cmax, AUC and T1/2. Enhances the effect.

Glipizide. Propranolol enhances the effect. When used in combination, dose adjustment may be required.

Glucagon. Administration of glucagon against the background of propranolol can lead to severe tachycardia and increased blood pressure.

Guanfacine. When guanfacine is used concomitantly with propranolol, the risk of developing or worsening bradycardia, AV block, cardiac arrest and heart failure increases.

Dextromethorphan + Paracetamol + Pseudoephedrine + [Ascorbic acid]

Propranolol, when used in combination, may enhance the vasoconstrictor effect of pseudoephedrine (as part of the combination dextromethorphan + paracetamol + pseudoephedrine + [ascorbic acid]).

Digoxin. Strengthens (mutually) the inhibition of AV conduction.

Diltiazem. Concomitant use of propranolol and intravenous administration of diltiazem is contraindicated.

Diltiazem. Strengthens (mutually) the negative chrono-, ino- and dromotropic effects. Against the background of diltiazem, the bioavailability of propranolol increases.

Dobutamine. Reduces (mutually) cardiac effects. Against the background of dobutamine, an increase in peripheral vascular resistance is possible.

Dronedarone. In clinical studies, bradycardia was observed more frequently with the combination of dronedarone and propranolol.

It is recommended to use propranolol with caution in combination with dronedarone due to pharmacokinetic and possible pharmacodynamic interactions (risk of additive inhibitory effects on the sinus and AV nodes). It is necessary to start treatment with metoprolol with low doses and increase their dose only under ECG monitoring. In patients already receiving propranolol, the addition of dronedarone should be monitored by ECG and the dose of propranolol adjusted if necessary.

Indapamide. Strengthens (mutually) the antihypertensive effect.

Interferon alpha. Combined use with interferon alfa in the form of an injection solution may lead to changes in the metabolism of propranolol.

Interferon alpha-2b. Interferon alfa-2b is able to reduce the activity of cytochrome P450 and, therefore, interfere with the metabolism of propranolol.

Captopril. Propranolol enhances the (mutually) hypotensive effect.

Clonidine. The combined use of propranolol with clonidine increases the risk of an excessive decrease in blood pressure.

Levothyroxine sodium. Reduces the activity of T4 5-deiodinase, although the levels of T3 and T4 change slightly. Against the background of levothyroxine sodium (when hypothyroidism turns into a euthyroid state), the effect may be weakened.

Lidocaine. Propranolol, when used in combination, reduces the clearance of lidocaine and increases its concentration in plasma.

Lidocaine. Propranolol reduces the hepatic clearance of lidocaine (decreased metabolism due to inhibition of microsomal liver enzymes and decreased hepatic blood flow) and increases the risk of toxic effects.

Lidocaine + Chlorhexidine. Propranolol reduces the hepatic clearance of lidocaine (as part of a combination of lidocaine + chlorhexidine in the form of a topical spray) - decreased metabolism due to inhibition of microsomal oxidation and decreased hepatic blood flow - and increases the risk of toxic effects (including drowsiness, drowsiness, bradycardia, paresthesia, etc.).

Lorazepam. When used in combination, propranolol increases plasma levels of lorazepam.

Maprotiline. Maprotiline is metabolized primarily by the CYP2D6 isoenzyme. Concomitant use of maprotiline with the beta-blocker propranolol, which is an inhibitor of the CYP2D6 isoenzyme, may lead to an increase in the plasma concentration of maprotiline. In such cases, it is recommended to monitor the plasma concentration of maprotiline and adjust the dose if necessary.

Metamizole sodium. Propranolol slows down biotransformation and increases the effect of metamizole sodium.

Metamizole sodium + Pitophenone + Fenpiverinium bromide. When used together, propranolol (slows down the inactivation of metamizole sodium) enhances the effect of the combination of metamizole sodium + pitofenone + fenpiverinium bromide.

Metamizole sodium + Triacetonamine-4-toluenesulfonate. Propranolol slows down the inactivation of metamizole sodium (as part of the combination metamizole sodium + triacetonamine-4-toluenesulfonate) and enhances its effect.

Metamizole sodium + Quinine. Propranolol enhances the effect of the combination of metamizole sodium + quinine.

Methyldopa. When propranolol is used concomitantly with methyldopa, the risk of developing or worsening bradycardia, AV block, cardiac arrest and heart failure increases.

Methyldopa. Propranolol enhances the (mutually) antihypertensive effect.

Mivacurium chloride. Propranolol enhances the effect, incl. the ability to unmask and increase the severity of myasthenia gravis.

Naproxen. The antihypertensive effect of propranolol is weakened by naproxen.

Naproxen + Esomeprazole. Naproxen (as part of the naproxen + esomeprazole combination) may reduce the antihypertensive effect of propranolol.

Nitroglycerine. Strengthens (mutually) the hypotensive effect.

Nifedipine. The simultaneous use of propranolol and nifedipine can lead to a significant decrease in blood pressure.

Octreotide. With octreotide, the likelihood of developing severe bradycardia, arrhythmias and conduction disturbances increases.

Pasireotide. It is recommended to monitor heart rate when prescribing pasireotide to patients receiving propranolol, which causes bradycardia, as concomitant therapy.

Pentaerythrityl tetranitrate. When used in combination, propranolol enhances the antianginal effect of pentaerythrityl tetranitrate.

Pilocarpine. Against the background of systemic action of pilocarpine, the risk of conduction disorders increases.

Pyridostigmine bromide. When used in combination, propranolol weakens the effects of pyridostigmine bromide.

Piroxicam. Against the background of piroxicam, the hypotensive effect is weakened, although the concentration of the free fraction in plasma increases (it is displaced from protein binding).

Propaphenone. Against the background of propafenone (CYP2D6 substrate), biotransformation is blocked, plasma concentration increases significantly, and T1/2 is prolonged.

Propylthiouracil. Against the background of propylthiouracil, the effects change; when administered in combination, a dose adjustment of propranolol may be required.

Reserpine. When reserpine is used concomitantly with propranolol, the risk of developing or worsening bradycardia, AV block, cardiac arrest and heart failure increases.

Repaglinide. Propranolol enhances the hypoglycemic effect; may camouflage some symptoms of hypoglycemia.

Risperidone. Strengthens (mutually) the antihypertensive effect.

Rifampicin. Rifampicin, when used in combination, shortens the T1/2 half of propranolol.

Rifapentine. Rifapentine may increase the metabolism and decrease the activity of propranolol; When used concomitantly with rifapentine, a dose adjustment of propranolol may be required.

Salmeterol. Propranolol weakens the effect; may cause bronchospasm in patients with asthma.

Simaldrat. Against the background of simaldrat, the absorption of propranolol decreases; when administered in combination, the interval between doses should be at least 2 hours.

Sulfasalazine. Sulfasalazine, when used in combination, increases the plasma concentration of propranolol.

Terazosin. Propranolol enhances the (mutually) hypotensive effect; with combined administration, a significant decrease in blood pressure is possible, requiring a dose reduction.

Terbutaline. Propranolol weakens the effect and can cause bronchospasm in patients with asthma.

Thiamine. Thiamine, when used in combination, reduces the pharmacological activity of propranolol.

Thioridazine. Concomitant use of propranolol (100-800 mg daily) and thioridazine causes an increase in plasma levels of thioridazine (approximately 50-400%) and its metabolites (approximately 80-300%); Concomitant use of propranolol and thioridazine should be avoided.

Trifluoperazine. With the simultaneous administration of trifluoperazine with propranolol, an increase in the concentration of both drugs is observed.

Ubidecarenon. Concomitant use of propranolol may lead to a decrease in plasma concentrations of ubidecarenone.

Felodipine. Felodipine increases the bioavailability of propranolol; when used in combination, propranolol enhances the hypotensive effect of felodipine.

Phenylephrine. Propranolol may have an unpredicted increase in the hypertensive effect (one report reported a sharp rise in blood pressure).

Phenytoin. The combined use of propranolol with phenytoin increases the severity of the cardiodepressive effect and the risk of lowering blood pressure.

Fluvoxamine. Fluvoxamine, when used in combination, increases the concentration of propranolol in the blood plasma.

Fluvoxamine. Against the background of fluvoxamine, the plasma level of propranolol increases (5 times).

Fosinopril. With simultaneous use, propranolol enhances the hypotensive effect of fosinopril. The bioavailability of fosinopril does not change when used concomitantly with propranolol.

Cimetidine. Cimetidine, when used in combination, increases the concentration of propranolol in plasma.

Cisatracurium besylate. When used in combination, propranolol enhances the effect of cisatracurium besylate. In rare cases, propranolol can worsen the course or promote the manifestation of latent myasthenia gravis, as well as cause myasthenic syndrome; as a result, increased sensitivity to cisatracurium besylate may occur.

Ethanol. The combined use of propranolol with ethanol increases the risk of central nervous system depression.

Overdose of the drug Propranolol, symptoms and treatment

Symptoms of propranolol intoxication depend on the patient's initial condition. In severe heart failure, even low doses of propranolol can cause signs of overdose; symptoms of damage to the digestive tract, cardiovascular system and central nervous system predominate. Possible feelings of fatigue, loss of consciousness, mydriasis, sometimes convulsions, arterial hypotension, bradycardia up to asystole, bronchospasm, hypoglycemia, shock. To eliminate the symptoms of overdose, intravenous administration of 1–2 mg of atropine is indicated, as well as the use of drugs with β-sympathomimetic activity (dopamine, dobutamine, isoprenaline, orciprenaline, epinephrine). Glucagon should first be administered intravenously at a dose of 0.2 mg/kg, then increase the dose to 0.5 mg/kg over 12 hours.

List of pharmacies where you can buy Propranolol:

Moscow
Saint Petersburg