β adrenergic receptor ( IC50 = 12 nM )

体外活性：盐酸普萘洛尔是一种非选择性β-肾上腺素能受体(βAR)拮抗剂，对β1AR和β2AR具有高亲和力，Ki值分别为1.8 nM和0.8 nM。盐酸普萘洛尔抑制 [3H]-DHA 与大鼠脑膜制剂的结合，IC50 为 12 nM。盐酸普萘洛尔用于控制高血压、嗜铬细胞瘤、心肌梗塞、心律失常、心绞痛和肥厚性心肌病。

盐酸普萘洛尔（口服；40 mg/kg；每日）相对于载体处理的植入物显着减小血管直径，并增加 IH Matrigel 植入物内表达磷酸化 ERK1/2 的细胞数量 [4]。

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心得安对IH异种移植小鼠模型血管发育的影响 [4]
为了评估心得安对体内造血干细胞和IH发育的影响，我们采用了先前描述的小鼠模型[20]。在IH小鼠模型中，将在Matrigel中重悬的HemSCs植入免疫功能低下的小鼠皮下，IH血管的发育进展超过3周。小鼠每日给予心得安或对照药40 mg/kg。使用1/12的表面积转换因子[37-39]，小鼠每天接受3.3-4.8 mg/kg的人体等效剂量。通过多普勒超声测量，心得安处理小鼠的IH Matrigel植入物在植入后14天和21天的血流量与对照组相比有所减少(数据未显示；图7 a)。21天IH Matrigel植入物的组织学分析（图7B）表明，与载体处理的植入物相比，普pranolol不影响血管密度（图7C），但确实显著降低了血管直径（图7D）。心得安治疗组血管直径减小与多普勒可检测血流损失相关。心得安还显著增加了IH Matrigel植入物中表达磷酸化ERK1/2的细胞数量（图7E），这与我们的体外研究结果一致。因此，心得安改善了与MAPK通路激活相关的IH小鼠模型中的血管发育。[4]

Caspase-3检测[4]
将HemSCs接种于含20% FBS培养基的EGM-2中，静置4小时。在0.1% FBS的SFM中，浓度递增的propranolol/普萘洛尔处理HemSCs 24小时。收集蛋白裂解物，使用caspase-3人酶联免疫吸附测定试剂盒（caspase-3 Human ELISA Kit）定量caspase-3的活化。

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cAMP测定[4]
使用LANCE Ultra cAMP试剂盒测定HemSCs中的cAMP水平。将HemSCs洗涤并在提供的刺激缓冲液（Hanks平衡盐水溶液、牛血清白蛋白、异丁基甲基黄嘌呤、HEPES缓冲盐水溶液）中重悬，并在96孔板上播种（每孔1000粒）。然后用药物治疗这些细胞30分钟。加入示踪剂和抗光camp工作液，室温孵育1小时。时间分辨荧光共振能量转移信号使用EnVision多标签平板阅读器进行测定。使用标准曲线确定cAMP水平，并使用综合曲线拟合（非线性回归）和Prism对数据进行插值。每种条件一组三次，实验至少进行两次。图中给出了一个有代表性的实验。 为了确定βARs在HemSCs中是否与Gαs或Gαi偶联，我们用异丙肾上腺素（含或不含10 μM福斯可林）在6倍剂量范围内连续用水稀释30分钟。接下来，按照描述测量cAMP水平，以确定HemSCs中βARs是否与Gαs或Gαi偶联。

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ERK1/2 Western Blotting [4]
细胞在纤维连接蛋白包被的板上培养，用不同浓度的βAR拮抗剂处理，孵育30分钟。细胞在TENT缓冲液（50 mM Tris [pH 8.0], 2 mM EDTA, 150 mM NaCl, 1% Triton-X-100）中裂解，其中含有1% Halt蛋白酶抑制剂，1%磷酸酶抑制剂和0.5%正钒酸钠。对ERK1/2 （p44/42, 1:10 00）和pERK1/2 （P-p44/42, 1:50 00）进行Western blotting。将印迹剥离，然后检测α-微管蛋白（1:10 000），使蛋白负载正常化。实验至少进行了三次，并在图中给出了一个有代表性的实验。

在体外，用不同浓度的不同药物处理新生小鼠心肌细胞（NMCM），包括异丙肾上腺素（0、1、2.5、5、10、20和50μM）；胺碘酮（0、1、2.5、5、10、20 和 50 μM）；美托洛尔（0、10、20、30、50、100、150 和 200 μM）；普萘洛尔（0、10、20、40、50 和 100 μM）；利多卡因（0、1、2.5、5、10、20 和 50 μM）；维拉帕米（0、1、2.5、5、10、20 和 50 μM）；伊伐布雷定（0、1、2、3、5、10 和 20 μM）。并选择促进CMs增殖最显着的药物浓度进行后续实验，包括异丙肾上腺素（10μM）、胺碘酮（5μM）、美托洛尔（20μM）、普萘洛尔（20μM）、利多卡因（5μM）、维拉帕米（5μM）。 2.5 μM)、伊伐布雷定 (3 μM) 用于 NMCM、NMCF 和 hPSC-CM。

A xenograft mouse model of IH (infantile hemangiomas) with HemSC cells
40 mg/kg
Orally administration; 40 mg/kg; daily

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IH Mouse Model [4]
To study the effects of propranolol on HemSCs in vivo, a xenograft mouse model of IH was used as previously described. In brief, 1.5 × 106 HemSCs (n = 2) suspended in 200 µL of Corning Matrigel Matrix was implanted subcutaneously into the flanks of female 6–8-week-old NCrNude immunodeficient mice. Propranolol, which was provided in drinking solution, was initiated the day of IH xenografting. Propranolol was diluted to 270 µM in 5% dextrose water (vehicle), and daily consumption was measured to calculate the treatment dosage, which averaged 40 mg/kg daily. Blood flow within the IH Matrigel implant was analyzed using a VEVO 2100 Ultrasound Imaging System on a Doppler setting on days 14 and 21 of IH development. The mice were anesthetized with isoflurane and restrained in a supine position. The region of interest was fully scanned, with the transducer positioned at its largest longitudinal section over the implant to optimize the spatial resolution of the image, maximizing the detail. Next, two-dimensional images were captured in uniform steps of 0.05 mm. The images of blood flow were analyzed using software provided by VisualSonics. The mice were sacrificed after 21 days. The Matrigel implants were collected and fixed overnight at 4°C in 10% formalin. The implants were dehydrated and embedded in paraffin for histological analysis. Vessel density and caliber were counted in 3–4 HPFs per implant (n = 4 for each group). Vessel density was determined as the number of vessels (whether longitudinally or axially oriented) per HPF. The vessel diameter was measured according to the orientation. For longitudinally oriented vessels, the width was measured at three points and averaged, and the cross-section (axial) vessels were measured once. Vessels were identified as tubular structures with erythrocytes within.

Absorption, Distribution and Excretion
Studies in man and experimental animals indicate that rapid hepatic clearance is responsible for appearance of only trace amount of unmetabolized propranolol in blood after small oral doses. With larger doses, blood levels are linearly related to dose, suggesting saturation of hepatic metabolic system.
Propranolol is almost completely absorbed from the GI tract; however, plasma concentrations attained are quite variable among individuals. There is no difference in the rate of absorption of the 2 isomers of propranolol. Propranolol appears in the plasma within 30 min, and peak plasma concentrations are reached about 60-90 min after oral administration of the conventional tablets. The time when peak plasma concentrations are reached may be delayed, but concentrations are not necessarily lowered, when the drug is administered with food. Oral bioavailability of the drug may be increased in children with Down's syndrome; higher than expected plasma propranolol concentrations have been observed in such children. Bioavailability of a single 40-mg oral dose of propranolol hydrochloride as a conventional tablet or oral solution reportedly is equivalent in adults.
Propranolol hydrochloride is slowly absorbed following administration of the drug as extended release capsules, and peak blood concentrations are reached about 6 hr after administration. When measured at steady state over a 24 hr period, the area under the plasma concentration time curve for the extended release capsules is about 60-65% of the plasma concentration time curve for a comparable divided daily dose of the conventional tablets. The lower plasma concentration time curve is probably caused by the slower rate of absorption of the drug from the extended release capsules with resultant greater hepatic metabolism. After administration of a single dose of propranolol as the extended release capsules, blood concentrations are fairly constant for about 12 hr and then decline exponentially during the following 12 hr.
Following iv administration of propranolol, the onset of action is almost immediate. Animal studies indicate that propranolol is rapidly absorbed after im administration.
For more Absorption, Distribution and Excretion (Complete) data for PROPRANOLOL HYDROCHLORIDE (12 total), please visit the HSDB record page.

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Metabolism / Metabolites
Besides ... 4-hydroxypropranolol and naphthoxylacetic acid, 6 new urinary metabolites have... been identified... /which are/ n-deisopropylpropranolol; 1-(alpha-naphthoxy)-2,3-propyleneglycol; ring hydroxylated 1-(alpha-naphthoxy)-2,3-propyleneglycol; alpha-naphthoxyacetic acid; alpha-naphthol and 1,4-dihydroxynaphthalene.
Isopropylamine and hexadeuteriated isopropylamine have been identified as urinary metabolites of propranolol and hexadeuteriated propranolol, respectively; this is believed to be 1st recorded example of single-step oxidative deamination of n-isopropylamine compound.
During initial oral therapy (but not during iv or chronic oral therapy), an active metabolite, 4-hydroxypropranolol, is formed. 4-Hydroxypropranolol has about the same beta-adrenergic blocking potency as does propranolol and may be present in plasma in amounts about equal to propranolol. This metabolite is eliminated more rapidly than propranolol and is virtually absent from the plasma 6 hr after oral administration of the drug. Results of one study indicate that after iv administration or chronic oral administration of propranolol, 4-hydroxypropranolol is not formed to a substantial extent, and beta-adrenergic blocking activity is more closely reflected by propranolol concentrations. Individual variations in ability to hydroxylate propranolol to the active metabolite may also exist. In addition, some other metabolites of propranolol may possess antiarrhythmic activity without beta-adrenergic blocking activity.
Propranolol is almost completely metabolized in the liver and at least 8 metabolites have been identified in urine. Only 1-4% of an oral or iv dose of the drug appears in feces as unchanged drug and metabolites.

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Biological Half-Life
When usual therapeutic doses of propranolol are administered chronically, the half-life ranges from 3.4-6 hr. Single dose studies generally have shown a shorter half-life of 2-3 hr.

Toxicity Summary
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 alcohol; slightly soluble in chloroform; practically 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 crisis; together 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 seen; spasm 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.

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because of the low levels of propranolol in breastmilk, amounts ingested by the infant are small and would not be expected to cause any adverse effects in breastfed infants. Studies during breastfeeding have found no adverse reactions in breastfed infants clearly attributable to propranolol. No special precautions are required. Propranolol has been used successfully in cases of persistent pain of the breast during breastfeeding.
◉ Effects in Breastfed Infants
A study of mothers taking beta-blockers during nursing found a numerically, but not statistically significant increased number of adverse reactions in those taking any beta-blocker. Although the ages of infants were matched to control infants, the ages of the affected infants were not stated. Of 8 mothers taking propranolol, one reported sleepiness in her breastfed infant, but she was also taking other unspecified drugs for hypertension.
A case of bradycardia in a 2-day-old breastfed infant was reported to the French pharmacovigilance system. However it is not clear from the report whether the mother had been taking propranolol near term and might have transmitted the drug to the infant transplacentally.
◉ Effects on Lactation and Breastmilk
Relevant published information on the effects of beta-blockade or propranolol during normal lactation was not found as of the revision date. A study in 6 patients with hyperprolactinemia and galactorrhea found no changes in serum prolactin levels following beta-adrenergic blockade with propranolol.

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Interactions
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.

[1]. Distinct signaling profiles of beta1 and beta2 adrenergic receptor ligands toward adenylyl cyclase and mitogen-activated protein kinase reveals the pluridimensionality of efficacy. Mol Pharmacol . 2006 Nov;70(5):1575-84.

[2]. Evidence against beta-adrenoceptor blocking activity of diltiazem, a drug with calcium antagonist properties. Br J Pharmacol. 1980 Aug;69(4):669-73.

[3]. Propranolol. Profiles Drug Subst Excip Relat Methodol. 2017;42:287-338.

[4]. Propranolol Targets Hemangioma Stem Cells via cAMP and Mitogen-Activated Protein Kinase Regulation. Stem Cells Transl Med. 2016 Jan;5(1):45-55.

Therapeutic Uses
Adrenergic beta-Antagonists; Anti-Anxiety Agents; Anti-Arrhythmia Agents; Antihypertensive Agents; Sympatholytics; Vasodilator Agents
/SRP: Former use/: Propranolol has proven to be effective in numerous cases in which digitalis, with or without quinidine and/or procainamide, failed to reduce ventricular rate, and in cases of paroxysmal atrial tachycardia attributed to digitalis toxicity.
Propranolol is also used in hypertrophic obstructive cardiomyopathies. In these conditions forceful contraction of myocardium along a ventricular outflow tract can greatly increase outflow resistance, particularly during exercise. .../It/ is sometimes useful in management of tachycardia and arrhythmias in patient with pheochromocytoma.
Medication (Vet): ...Atropine in conjunction with propranolol /was found/ to be useful in treatment of oleander poisoning.
For more Therapeutic Uses (Complete) data for PROPRANOLOL HYDROCHLORIDE (25 total), please visit the HSDB record page.

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Drug Warnings
.../Propranolol/ is relatively contraindicated in ...hay fever, cardiogenic shock, congestive heart failure, right ventricular failure secondary to pulmonary hypertension, and when myocardial depressant anesthetics, tricyclic antidepressants, or oral hypoglycemics are used.
Propranolol (1% solution) used as eye-drops .../per 1 report/, caused intense pain lasting as long as 15 min and induced hyperemia and slight miosis, but according to others these eye-drops have been well tolerated by most patients in use up to 4 times/day for 3-4 months, causing burning sensations and conjunctival hyperemia in only 8/47 eyes.
Contraindicated in patients with cardiogenic shock, sinus bradycardia and greater than first degree block, bronchial asthma, and congestive heart failure. Adverse reactions include weakness, light headedness, depression, bradycardia, paresthesia of hands, arterial insufficiency (e.g., Raynaud type), nausea, and diarrhea. Use is best avoided in patients with bronchospastic diseases and therapy in diabetic patients must be closely monitored.
After sudden cessation of propranolol therapy in some patients treated for angina, increased frequency, duration, and severity of angina episodes have occurred, often within 24 hr. These episodes are unstable and are not relieved by nitroglycerin. Acute and sometimes fatal myocardial infarction and sudden death have also occurred after abrupt withdrawal of propranolol therapy in some patients treated for angina. In hypertensive patients, sudden cessation of propranolol has produced a syndrome similar to florid thyrotoxicosis, characterized by tenseness, anxiety, tachycardia, and excessive perspiration; these symptoms occurred within one week of cessation of the drug and were relieved by reinstituting propranolol therapy.
For more Drug Warnings (Complete) data for PROPRANOLOL HYDROCHLORIDE (31 total), please visit the HSDB record page.

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1 The isolated spontaneously beating atria of the rat, diltiazem (0.01 to 0.1 microM) shifted the atrial rate concentration-response curves to isoprenaline to the right in a non-parallel manner and depressed their maxima. Under the same experimental conditions, (+/-)-propranolol (0.03 to 0.1 microM) behaved as a competitive beta-adrenoceptor antagonist. 2 Whereas (+/-)-propranolol (IC50 = 12 nM) and isoprenaline (IC50 = 0.9 microM) inhibited (-)-[3H]-dihydroalprenolol binding to rat brain membrane preparations, diltiazem failed to do so in concentrations up to 10 microM. 3 Diltiazem but not (+/-)-propranolol, antagonized the positive chronotropic responses to calcium in spontaneously beating rat atria. 4 It is proposed that diltiazem inhibited the tachycardia induced by isoprenaline through an effect on calcium which may be an essential modulator of the sequence of events linking the beta-adrenoceptor activation and heart rate response.[2]

C16H22CLNO2

295.8

331.11

C, 64.97; H, 7.50; Cl, 11.98; N, 4.74; O, 10.82

318-98-9

(S)-(-)-Propranolol hydrochloride; 4199-10-4; Propranolol; 525-66-6; Propranolol-d7 hydrochloride; 1613439-56-7; Propranolol-d7 (ring-d7); 344298-99-3

62882

White to off-white solid powder

434.9ºC at 760mmHg

163-165 °C(lit.)

216.8ºC

3.77

41.49

3

3

6

20

257

0

OC(CNC(C)C)COC1=CC=CC2=CC=CC=C12.Cl

ZMRUPTIKESYGQW-UHFFFAOYSA-N

InChI=1S/C16H21NO2.ClH/c1-12(2)17-10-14(18)11-19-16-9-5-7-13-6-3-4-8-15(13)16;/h3-9,12,14,17-18H,10-11H2,1-2H3;1H

1-naphthalen-1-yloxy-3-(propan-2-ylamino)propan-2-ol;hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: 25 mg/mL (84.52 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。

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配方 2 中的溶解度: 5%DMSO + Corn oil: 3.0mg/ml (10.14mM)

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。