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(±)-[2-Hydroxy-3-(naphthyloxy)propyl]isopropylammoniumchlorid
AURORA KA-6762 · PROPRANOLOL HCL · dl-propranolol hcl · dl-propranololHClbp · (+/-)-PROPANOLOL HCL · DL-PROPRANOLOL HCL 99% · PROPANOLOL HYDROCHLORIDE · PENTAPROPANOLOLHYDROCHLORIDE
![Molekülstruktur von (±)-[2-Hydroxy-3-(naphthyloxy)propyl]isopropylammoniumchlorid](/img/chemical/62882.png)
Identifikatoren & physikalische Daten
| CAS No. | 318-98-9 |
|---|---|
| Summenformel | C16H21NO2.ClH |
| Durchschnittliche Molmasse | 295,8 g/mol |
| Monoisotopische Masse | 295,13390662 g/mol |
| SMILES | CC(C)NCC(O)COc1cccc2ccccc12.Cl |
| InChIKey | ZMRUPTIKESYGQW-UHFFFAOYSA-N |
| PubChem CID | 62882 |
| ChEMBL | CHEMBL1671 |
| EC No. | 206-268-7 |
| DTXSID | DTXSID3021198 |
| Lokaler Name | (±)-[2-Hydroxy-3-(naphthyloxy)propyl]isopropylammoniumchlorid |
Chemische & physikalische Eigenschaften
| Polarare Oberfläche (TPSA) | 41,5 |
|---|---|
| H-Brücken-Donoren | 3 |
| H-Brücken-Akzeptoren | 3 |
| Frei drehbare Bindungen | 6 |
| Schwere Atome | 20 |
| Formalladung | 0 |
| Komplexität | 257 |
| LogP (Verteilungskoeffizient) | log Kow = -0.45 @ pH 2.0 |
| Geruch | Odorless |
| Geschmack | Bitter |
| Color/Form | White or almost white powderSolidCrystals from n-propanol |
| Löslichkeit | Practically insoluble in ether, benzene, ethyl acetate>44.4 [ug/mL] (The mean of the results at pH 7.4)H2O: 50 mg/mL, clear, colorless |
| Human Drugs | Breast FeedingLactationMilk, HumanAntihypertensive AgentsAdrenergic Beta-AntagonistsAntiarrhythmicsFDA approved drugs -> Active ingredientEMA approved medicines: Human medicine |
| Decomposition | When heated to decomposition it emits toxic fumes of oxides of nitrogen. |
| Schmelzpunkt | 163-164 °C163-165 °C(lit.) |
| Stability/Shelf Life | IT IS STABLE TO HEAT, UNSTABLE TO LIGHT. /HYDROCHLORIDE/Propranolol hydrochloride preparations should be protected from light and storedat room temperature (approximately 25 °C). The manufacturer recommends that propranolol hydrochloride extended-release capsules be stored in tight, light resistant containers and be protected from moisture, freezing, and excessive heat. USP recommends that propranolol hydrochloride preparations be stored in well closed containers. Solutions of the drug have maximum stability at pH 3 and decompose rapidly at alkaline pH. Decomposition in aqueous solution is accompanied by a lowered pH and discoloration. Propranolol hydrochloride injection is reportedly compatible with 0.9% sodium chloride injectionhowever, specialized references should be consulted for specific compatibility information. |
| Dissociation Constants | pKa = 9.45 |
| Other Experimental Properties | Intense mass spectral peaks: 72 m/z, 100 m/z, 144 m/z, 259 m/z /Propranolol/ |
| Lagerbedingungen | 2-8°C |
| Aggregatzustand | powder |
| Farbe | white |
| InChI | 1S/C17H23NO2.ClH/c1-13(2)10-18-11-15(19)12-20-17-9-5-7-14-6-3-4-8-16(14)17/h3-9,13,15,18-19H,10-12H2,1-2H31H |
| InChIKey | RTTYPFXTLKDXPS-UHFFFAOYSA-N |
| CAS Datenbank | 3506-09-0(CAS DataBase Reference) |
Sicherheit & Vorschriften
| GHS-Einstufung | WarningH302 (98.7%): Harmful if swallowed [Warning Acute toxicity, oral]P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 153 reports by companies from 12 notifications to the ECHA C&L Inventory.H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral] |
|---|---|
| Regulatorische Informationen | Chemical: 2-Propanol, 1-[(1-methylethyl)amino]-3-(1-naphthalenyloxy)-, hydrochloride (1:1)Propranolol hydrochloride: Does not have an individual approval but may be used under an appropriate group standard |
| FDA-Anforderungen | The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl propranolol hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended21 U.S.C. 321-392). |
| Special Reports | Feenstra MGFunctional Neuroteratology of Drugs Acting on Adrenergic Receptors. Neurotoxicology 13 (1): 55-63 (1992). Long term biochemical, morphological, behavioral and electrophysiological effects have been reported after pre- or postnatal exposure of rats to adrenergic drugs, the alpha 2-agonist clonidine and the beta-antagonist propranolol in particular, and are summarized here.Hjalmarson A, Olsson GMyocardial Infarction. Effects of Beta-blockade. Circulation 84 (6 Suppl): VI101-7 (1991). In this review article, different aspects of early and late treatment with beta-adrenoceptor blockers are discussed. Impressive effects on mortality and morbidity have been obtained with propranolol, timolol, and metoprolol, which are noncardioselective as well as more beta 1-selective (metoprolol), but they are all lacking intrinsic sympathomimetic activity and, furthermore, have a relatively high degree of lipophilicity.Huang SK, Marcus FIBeta-blockers, Phenytoin, and Calcium Antagonists. Hosp Ther 12 (Jun): 66, 71-73, 77 (1987). A brief review of the unique roles of beta-adrenergic blockers, including propranolol, metoprolol, and acebutolol, phenytoin and verapamil, in the treatment of ventricular arrhythmias is presented including their dosages and side effects profile.Lader MBeta-adrenoceptor Antagonists in Neuropsychiatry: An Update. J Clin Psychiatry 49 (6): 213-23 (1988). In this overview, which concentrates on the recent literature, four indications for use of the beta- adrenoceptor antagonists, including propranolol, are reviewed, with particular reference to efficacy, mode of action, and clinical utility.McAinsh J, Cruickshank JMBeta-blockers and Central Nervous System Side Effects. Pharmacol Ther 46 (2): 163-97 (1990). Every published clinical paper, in which the beta-blockers propranolol, pindolol, metoprolol, and atenolol were compared, was assessed for information pertaining to CNS side effects. |
| Hazard Classes and Categories | Acute Tox. 4 (100%)Acute Tox. 4 (98.7%) |
| Entsorgungsverfahren | SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air qualitypotential migration in soil or watereffects on animal, aquatic, and plant lifeand conformance with environmental and public health regulations. |
| Körperbelastung | The drug is distributed into milk. |
| Wechselwirkungen | Propranolol antagonizes cardiac stimulation that may limit effectiveness of hydralazine, and combination has been shown to be more effective than either drug alone.Neuromuscular blockade produced by tubocurarine was prolonged in 2 thyrotoxic patients receiving high doses (120 mg/day for 14 days) of propranolol. ...Decamethonium and succinylcholine have been shown to interact with propranolol in similar manner... in animals.Propranolol increased acute CNS toxicity of ether, hexobarbital, morphine and urethane in mice.Stimulatory effect of epinephrine on heart is blocked by propranolol. If epinephrine is administered to patient receiving propranolol, reflex tachycardia may result, /SRP: due to fall in blood pressure because of beta blockade on blood vessels/.For more Interactions (Complete) data for PROPRANOLOL HYDROCHLORIDE (16 total), please visit the HSDB record page. |
| Milk Concentrations | The drug is distributed into milk. |
| Toxizitätsübersicht | IDENTIFICATION: Propranolol is a class II antiarrhthmic drug which be longs to the beta-andrenergic blocking agents. Propranol hydrochloride is a white, odorless white crystalline powder. It is soluble in alcoholslightly soluble in chloroformpractically insoluble in ether. Cardiovascular diseases: Propranolol, a non cardioselective beta-blocker, is mostly used in the treatment of hypertension, angina, for the prevention of re-infarction in patients who have suffered from myocardial infarction. It is also used to control symptoms of anxiety and in the treatment of supraventricular tachycardia, hypertrophic obstructive and cardiomyopathy. Endocrine disorders: In hyperthyroidism and thyrotoxic crisistogether with alpha-blocking agents in the preoperative treatment of pheochromocytoma. Hepatic diseases: Prevention of hemorrhage in portal hypertension Neurological disorders: Propranolol has also been used in the treatment of extrapyramidal disorders and in the prophylaxis of migraine headache. Anxiety disorders: Propranolol may be used in acute stress reactions, somatic anxiety and panic reactions, but its value is questioned. HUMAN EXPOSURE: Main risks and target organs: Beta-blockers compete with endogenous and/or exogenous beta-adrenergic agonists. Propranolol is not cardioselective and it has no intrinsic sympathomimetic activity. It has membrane stabilizing properties and is highly lipid soluble. At toxic doses, propranolol has a pronounced negative chronotropic and inotropic effect and also a quinidine like effect on the heart. The cardiovascular system is the main target organ. Propranolol decreases sinus rate, atrio-ventricular conduction, intraventricular conduction and cardiac contractility. Central nervous system toxicity (coma and convulsions) may also occur because of its high liposolubility.Summary of clinical effects: Toxicity occurs within 1 to 2 hours following ingestion but the delay in onset may vary according to the formulation. Symptoms may include: Cardiovascular disturbances: bradycardia, atrioventricular block of varying degrees, intraventricular block, hypotension, cardiogenic shock and pulmonary edema. Neurological symptoms: coma and convulsions. Respiratory depression and apnea. Cardiovascular collapse and apnea may occur suddenly. Patients with underlying cardiovascular disease are predisposed to the adverse cardiac effects of propranolol. Propranolol may induce bronchospasm in asthmatic patients. Contraindications: Absolute: asthma, congestive cardiac failure, atrio-ventricular block, bradycardia and treatment with amiodarone. Relative: Raynaud's disease, diabetes mellitus. Routes of entry: Oral: Ingestion is the most frequent cause of poisoning Inhalation: no case has been reported. The effect of 10 mg propranolol given by nasal route is rapid and equivalent to the intravenous route. Parenteral: No case of overdoses has been reported. Cardiovascular symptoms have been reported after therapeutic administration. Absorption by route of exposure: After oral administration, propranolol is almost completely and rapidly absorbed from the gastrointestinal tract. However, because of the high first-pass metabolism and hepatic tissue binding, the absolute bioavailability is only about 30% and varies greatly between individuals. Peak plasma concentration occurs one to two hours after administration. After administration of the sustained release formulation, the peak plasma concentration occurs 7 hours after absorption. Distribution by route of exposure: About 90 to 95 % of the drug is bound to plasma proteins. Propranolol is highly lipophilic: it crosses the blood-brain barrier and the placenta. Biological half-life by route of exposure: After oral administration, propranolol undergoes saturable kinetics. The plasma half-life is 3 to 6 hours and is about 12 hours with the sustained release forms. The total body clearance is 800 mL/minute/1.73 m2. After overdose, the plasma half-life is prolonged. One study reported a half-life of 16 hours. In two cases reported, the half-life was 13.8 and 8.3 hours. In five cases, the mean plasma half-life was 10.5 hours (range: 5.1 to 17). Metabolism: Propranolol is extensively metabolized by the liver. At least one of the metabolites, the 4-hydroxypropranolol, is biologically active. The hepatic metabolism is saturable and bioavailability may be increased in overdoses. Elimination by route of exposure: After a single oral dose, propranolol is completely eliminated in 48 hours, mainly by hepatic metabolism. Less than 0.5 % is excreted unchanged in urine. The renal clearance is 12 mL/kg/minute. About 20% of the dose is eliminated in urine mainly as glucuronide conjugates. Propranolol is excreted in breast milk at a concentration of 50% that of blood. Mode of action Toxicodynamics: Propranolol is a non cardioselective beta-blocker with no intrinsic sympathomimetic action. It has membrane stabilizing activity and is highly lipid soluble. At toxic doses, propranolol has a pronounced negative chronotropic and inotropic effect and a quinidine-like effect on the heart: the result is a reduction of the heart rate, a decrease of the sino-atrial and atrioventricular conduction, a prolongation of the intraventricular conduction and a decrease of cardiac output. Blockade of beta-2 receptors may cause bronchospasm and hypoglycemia. Given its high lipid solubility, propranolol crosses the blood-brain barrier and may cause coma and convulsions. Pharmacodynamics: Beta-blocking agents compete with endogenous and/or exogenous beta-adrenergic agonists. Their specific effects depend on their selectivity for beta-1 receptors (located in the heart) or beta-2 receptors (located in bronchi, blood vessels, stomach, gut, uterus). Beta-blockers are classified according to their cardioselectivity, membrane stabilizing effect, intrinsic sympathomimetic effect and lipid solubility. At therapeutic doses, propranolol slightly decreases heart rate (15%), supraventricular conduction and cardiac output (15 to 20%). Cardiac work and oxygen consumption are also decreased. Propranolol decreases the secretion of renin. The pharmaceutical form of propranolol is a racemate: the dextrorotary isomer accounts for most of the beta-blocking effect, whereas the levorotary isomer has a predominantly membrane stabilizing effect. Toxicity: Human data: Adults: Propranolol toxicity shows individual variations which may be due to an underlying cardiac disease, to the ingestion of other cardiotoxic drugs and to variations in first-pass metabolism. Children: Ingestion of 70 mg by a 2 year old child produced drowsiness, second degree atrioventricular block and hypoglycemia. Ingestion of 100 mg by a 5-year-old child produced drowsiness, delirium and hallucinations. Interactions: Decreased bioavailability: Antacids decrease the gastric absorption of propranolol. Barbiturates, phenytoïn and rifampicin increase the first-pass clearance of propranolol by hepatic enzyme induction. Increased bioavailability: Plasma propranolol concentrations may be increased up to 50% by histamine H2 antagonists and oral contraceptives, which decrease hepatic metabolism by enzyme inhibition. Diminished pharmacodynamic effects: Non-steroidal anti-inflammatory drugs decrease the antihypertensive effect of propranolol. Nifedipine might exacerbate the symptoms of beta-blocker withdrawal. Enhanced pharmacodynamic effects: Digitalis, amiodarone, verapamil and diltiazem may increase bradycardia due to propranolol. Verapamil, prenylamine, flecainide and disopyramide enhance the negative inotropic effect of propranolol. Main adverse effects: Numerous adverse effects during propranolol treatment have been reported. Cardiovascular: sinus bradycardia, atrioventricular block, hypotension, increase of left ventricular failure, cardiogenic shock, intermittent claudication. Respiratory: bronchospasm, exacerbation of asthmatic symptoms in known asthmatics, pulmonary edema. Central nervous system: depression, psychosis, convulsions, hallucinations. Musculoskeletal: muscle weakness, aggravation of myasthenia gravis, peripheral neuropathy. Gastrointestinal: vomiting, diarrhea, dry mouth. Endocrine and metabolic: hypoglycemia, hyperkalemia, hypothyroidism, sexual dysfunction (impotence). Dermatological: urticaria, exfoliative dermatitis. Hematological: agranulocytosis (immunologic reaction), thrombocytopenia. Teratogenicity: a case of tracheoesophageal fistula in a newborn of a mother treated with propranolol during the pregnancy has been reported. However, a teratogenic effect of propranolol has not been confirmed. Pregnancy: hypoglycemia and lethargy have been reported in newborn from mothers treated with propranolol before delivery. Others: propranolol treatment may potentiate anaphylactic shock. Clinical effects: Acute poisoning: Ingestion: The severity of propranolol poisoning is due to its cardiotoxicity and depends on the dose ingested, the presence of underlying cardiac disease and concomitant ingestion of other cardiotoxic drugs. Symptoms and signs appear within one to two hours and may include the following: Cardiovascular effects: bradycardia, hypotension, cardiogenic shock. The ECG may show nodal rhythm, atrioventricular block and QRS widening. CNS effects: lethargy, coma and convulsions and mydriasis. Hypoventilation resulting from severe shock. Parenteral exposure: Cardiovascular effects: bradycardia, hypotension, cardiogenic shock. The ECG may show nodal rhythm, atrioventricular block and QRS widening CNS effects: lethargy, coma and convulsions, mydriasis Hypoventilation resulting from severe shock. Course, prognosis, cause of death: Patients who survive 48 hours after acute poisoning or who have not developed cardiac arrest before admission are likely to recover. Death may occur from cardiac asystole which is noted by hypoxemia. The prognosis depends on the dose ingested and is worse in patients with an underlying cardiac disease and in those who have ingested other cardiotoxic drugs. Systematic description of clinical effects: Cardiovascular: Acute: Cardiovascular symptoms are the major features of propranolol poisoning. Bradycardia is the commonest symptom (present in 60 to 90% of cases) and occurs soon after ingestion. Hypotension is observed in about 50 to 70% of the cases. Hypotension and shock are due to decreased cardiac output and vasodilatation. Cardiac arrest may occur within 1 to 2 hours of ingestion. Cardiac arrest has been reported to occur in 45 minutes following an over dose propranolol by a 60 year old man. ECG changes are always present in symptomatic poisoning: sinus or nodal bradycardia, atrioventricular block (1st to 3rd degree) are the most common. Widening of the QRS interval, bundle branch block or increased QT interval are less frequently observed. Respiratory: Acute: Respiratory depression and apnea is mostly associated with severe shock and is due to cerebral hypoxia. Pulmonary edema may occur, especially in patients with a previous compromised cardiac function. Bronchospasm may occur in susceptible patients. Neurological: CNS: Acute: Lethargy, drowsiness, agitation, delirium, hallucinations and mydriasis may be observed. Coma is usually only seen in patients with cardiovascular collapse. Convulsions have been reported after ingestion of large doses. Convulsions may be due to hypotension or to a direct effect of propranolol (membrane stabilizing effect). Chronic: Fatigue, CNS depression, hallucinations and psychosis have been reported. Autonomic nervous system: Acute: Effects of beta-receptor blockade. Chronic: Effects of beta-receptor blockade. Skeletal and smooth muscle: Chronic: Muscular fatigue may be observed. Gastrointestinal: Acute: vomiting, nausea may be seenspasm of the lower oesophageal sphincter has been reported in two cases. A case of mesenteric ischemia following propranolol overdose has been reported. Eye, ear, nose, throat: local effects: Acute: Mydriasis and diplopia may be noted. Metabolic: Acid-base disturbances: Metabolic acidosis may occur in severe poisoning with shock. Fluid and electrolyte disturbances: Hypokalemia or a hyperkalaemia have been reported rarely. Others: Hypoglycemia was reported in two cases of poisoning in children. |
| Human Toxicity Excerpts | /HUMAN EXPOSURE STUDIES/ Elevated sympathetic activity can modulate parameters of immunity. ... The role of the low sympathetic activity in resting healthy volunteers by treating them with the beta-adrenergic antagonist propranolol (3 x 40 mg/d for 7 days) /was investigated/. Propranolol treatment increased the number of circulating T cells but not that of other white blood cells. Similarly, Con A-stimulated lymphocyte proliferation and IL-2 formation were enhanced. Although the number of circulating NK cells did not change, NK-cell activity was reduced markedly after propranolol treatment. These alterations are not a mirror image of the changes observed under conditions of elevated sympathetic activity but demonstrate that withdrawal of the endogenous sympathetic tone by drugs such as propranolol can modulate parameters of human immunity./HUMAN EXPOSURE STUDIES/ Limited information is available on the acute toxicity of propranolol. In adults who intentionally ingested the drug, estimates of the ingested doses have ranged from 0.8-6 g. The principal manifestations of overdosage were bradycardia and severe hypotension (which may result in peripheral cyanosis)loss of consciousness and seizures have also occurred. Cardiac failure and bronchospasm may also occur. In most cases of acute propranolol overdosage, the patient recoveredhowever, in a few cases, toxicity was severe enough to result in death. Two small children who ingested a total of 150 mg of propranolol hydrochloride became drowsy, perspired, and experienced periods of sinoatrial node blockthey were treated with iv and oral dextrose. Severe hypertension has been reported in 8 patients with schizophrenic disorder who received propranolol in rapidly increasing doses (600 mg in the first 24 hr)these patients responded to iv phentolamine./CASE REPORTS/ A case of carpal tunnel syndrome in a hypertensive man on long term treatment with a beta-blocker, propranolol is described. The clinical and instrumental findings, including MRI at the wrist, excluded all other possible causes of carpal tunnel syndrome. The improvement in symptoms and electromyographic findings on discontinuation of the drug suggested that the carpal tunnel syndrome may have been related to the beta-blocker therapy./CASE REPORTS/ A case of severe propranolol intoxication that presented as an acute psychotic episode preceding cardiovascular decompensation and seizures by several hours /is reported/. Though acute reversible psychosis has been appreciated after initiating or increasing propranolol dosage therapeutically, this association has not been reported in the literature regarding beta-blocker overdose or intoxication. |
| Drug Induced Liver Injury | Drug Induced Liver Injury Rank (DILIrank 2.0)Propranolol hydrochlorideAmbiguous-DILI-concern3Warnings & precautionsDOI:10.1016/j.drudis.2016.02.015 |
| Non-Human Toxicity Excerpts | /LABORATORY ANIMALS: Acute Exposure/ Large doses /of propranolol/ have usually been found to be /CNS/ depressant in lab animals. ...Glycogenolysis in heart and skeletal muscle is inhibited by... beta-adrenergic blocking drugs. That in liver is /also/ inhibited ...in some species./LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ A total of 112 3 wk old Wistar rats were separated into eight groups: control groups I-IV (n = 62) and propranolol treated groups V-VIII (n = 50). Propranolol hydrochloride (100 mg/kg) was present in the rats' drinking water until 26 wk of age and growth rates of all groups were monitored daily until 53 days of age and thereafter every third day throughout the study. Chronic oral propranolol administration produced growth retardation (p< 0.05) in both sexes that was reversible when treatment was discontinued. Organ wt were generally smaller in propranolol treated ratson the other hand, the ratio of most organ wt per 100 g of body wt was greater in propranolol treated rats (especially females). The radio-immunological determination of plasma growth hormone showed increased concn of growth hormone in propranolol treated rats (p< 0.05), whereas hypothalamic somatostati content was not significantly changed. The results showed that the retarded growth rate following chronic oral propranolol administration to growing rats was independent of changes in plasma growth hormone and hypothalamic somatostatin concn, and that retardation was entirely reversible when the beta-adrenoceptor antagonist was discontinued./LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In dietary administration studies in which mice and rats were treated with propranolol for up to 18 months at doses of up to 150 mg/kg/day, there was no evidence of drug-related tumorigenesis./LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a study in which both male and female rats were exposed to propranolol in their diets at concentrations of up to 0.05%, from 60 days prior to mating and throughout pregnancy and lactation for two generations, there were no effects on fertility./GENOTOXICITY/ Based on differing results from Ames Tests performed by different laboratories, there is equivocal evidence for a genotoxic effect of propranolol in bacteria (S. typhimurium strain TA1538). |
| Antidote and Emergency Treatment | Emergency and supportive measures. 1. Maintain an open airway and assist ventilation if necessary. 2. Treat coma, seizures, hypotension, hyperkalemia, and hypoglycemia if they occur. 3. Treat bradycardia with atropine, 0.01-0.03 mg/kg IVisoproterenol (start with 4 ug/min and increase infusion as needed)or cardiac pacing. 4. Treat bronchospasm with nebulized bronchodilators. 5. Continuously monitor the vital signs and ECG for at least 6 hours after ingestion. /Propranolol, Beta-adrenergic blockers/Specific drugs and antidotes. 1. Bradycardia and hypotension resistant to ... /normal/ measures should be treated with glucagon, 5-10 mg IV bolus, repeated as needed and followed by an infusion of 1-5 mg/hr. Epinephrine (intravenous) infusion starting at 1-4 ug/min and titrating to effect. 2. Wide complex conduction defects caused by membrane-depressant poisoning may respond to sodium bicarbonate, 1-2 meq/kg, as given for tricyclic antidepressant overdose. 3. Torsades de pointes polymorphous ventricular tachycardia associated with QT prolongation resulting from sotalol poisoning can be treated with isoproterenol infusion, magnesium, or overdrive pacing. Correction of hypokalemia may also be useful. /Propranolol, Beta-adrenergic blockers/Decontamination. 1. Prehospital. Administer activated charcoal if available. 2. Hospital. Administer activated charcoal. Consider gastric lavage for large ingestions, especially involving propranolol. Gastric emptying is not necessary for small ingestions if activated charcoal can be given promptly. /Propranolol, Beta-adrenergic blockers/Enhanced elimination. Most beta blockers, especially the more toxic drugs such as propranolol, are highly lipophillic and have a large volume of distribution (Vd). For those with a relatively small volume of distribution coupled with a long half-life or low intrinsic clearance (eg, acebutolol, atenolol, nadolol, or sotalol), hemoperfusion, hemodialysis, or repeat-dose charcoal may be effective. /Propranolol, Beta-adrenergic blockers/For more Antidote and Emergency Treatment (Complete) data for PROPRANOLOL HYDROCHLORIDE (6 total), please visit the HSDB record page. |
| Effects During Pregnancy and Lactation | ◉ Summary of Use during Lactation |
| F | 10 |
| Wassergefährdungsklasse (WGK) | 3 |
| UN-Transportnummer | 3249 |
| RTECS-Nr. | UB7525000 |
| R-Sätze (R) | 22 |
| Gefahrensymbole | Xn |
| Gefahrenklasse | 6.1(b)Acute Tox. 4 Oral |
| Verpackungsgruppe | III |
| Lagerklasse | 11 - Combustible Solids |
Anwendungen & Verwendung
Verwenden
Adrenoceptor antagonist, anti-arrythmic