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Inderal (Propranolol)

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Inderal is an effective medication which helps to fight with hypertension and other heart or circulatory conditions. It is also taken to prevent heart attack and reduce severe headaches. Inderal acts by affecting the heart and circulation.

Other names for this medication:

Similar Products:
Propranolol, Innopran XL


Also known as:  Propranolol.


Inderal is a perfect remedy, which helps to fight against hypertension and other heart or circulatory conditions. Its target is to prevent heart attack and reduce severe headaches.

Inderal acts by affecting the heart and circulation. It is beta blocker.

Inderal is also known as Propranolol, Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Sumial, Anaprilinum.

Generic name of Inderal is Propranolol.

Brand names of Inderal are Inderal, Inderal LA, InnoPran XL.


The dosage of Inderal depends on your condition.

Take Inderal tablets and capsules every day at the same time orally with water.

Do not crush or chew it.

The extended-release (long-acting) tablet is usually taken once a day. Immediate-acting Inderal can be taken 2-4 times a day.

If you want to achieve most effective results do not stop taking Inderal suddenly.


If you overdose Inderal and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Inderal overdosage: shortness of breath, uneven heartbeats, seizure, weakness, fainting, dizziness, bluish-colored fingernails.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Inderal are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Inderal if you are allergic to Inderal components.

Do not take Inderal if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Be careful with Inderal if you are taking heart medicines (such as nifedipine (Procardia, Adalat), reserpine (Serpasil), verapamil (Calan, Verelan, Isoptin), diltiazem (Cartia, Cardizem)), MAO inhibitor (such as isocarboxazid (Marplan), tranylcypromine (Parnate), phenelzine (Nardil), or selegiline (Eldepryl, Emsam)),cold medicines, stimulant medicines or diet pills,medicine for asthma or other breathing disorders (such as albuterol (Ventolin, Proventil), bitolterol (Tornalate), metaproterenol (Alupent), pirbuterol (Maxair), terbutaline (Brethaire, Brethine, Bricanyl) and theophylline (Theo-Dur, Theolair)),a diabetes medication (such as insulin, glyburide (Diabeta, Micronase, Glynase), glipizide (Glucotrol), chlorpropamide (Diabinese), or metformin (Glucophage)), allergy medicine, guanabenz (Wytensin),clonidine (Catapres).

Be careful with Inderal if you suffer from or have a history of bradycardia (<50 beats/minute), uncontrolled congestive heart failure, sick sinus syndrome, atrioventricular block (2 or 3 degree), cocaine toxicity, asthma or chronic obstructive pulmonary disease (COPD), diabetes, depression, liver or kidney disease, myasthenia gravis, Raynaud's syndrome. You can take Inderal on the lower dose.

Be careful with Inderal if you are going to have a surgery.

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Inderal suddenly.

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To study the protective effect of oxyphenamone, a novel inodilator against myocardial ischemia-reperfusion injury.

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Experimental studies in preclinical mouse models of breast cancer have shown that chronic restraint stress can enhance disease progression by increasing catecholamine levels and subsequent signaling of β-adrenergic receptors. Catecholamines also signal α-adrenergic receptors, and greater α-adrenergic signaling has been shown to promote breast cancer in vitro and in vivo. However, antagonism of α-adrenergic receptors can result in elevated catecholamine levels, which may increase β-adrenergic signaling, because pre-synaptic α2-adrenergic receptors mediate an autoinhibition of sympathetic transmission. Given these findings, we examined the effect of α-adrenergic blockade on breast cancer progression under non-stress and stress conditions (chronic restraint) in an orthotopic mouse model with MDA-MB-231HM cells. Chronic restraint increased primary tumor growth and metastasis to distant tissues as expected, and non-selective α-adrenergic blockade by phentolamine significantly inhibited those effects. However, under non-stress conditions, phentolamine increased primary tumor size and distant metastasis. Sympatho-neural gene expression for catecholamine biosynthesis enzymes was elevated by phentolamine under non-stress conditions, and the non-selective β-blocker propranolol inhibited the effect of phentolamine on breast cancer progression. Selective α2-adrenergic blockade by efaroxan also increased primary tumor size and distant metastasis under non-stress conditions, but selective α1-adrenergic blockade by prazosin did not. These results are consistent with the hypothesis that α2-adrenergic signaling can act through an autoreceptor mechanism to inhibit sympathetic catecholamine release and, thus, modulate established effects of β-adrenergic signaling on tumor progression-relevant biology.

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Thrombin-induced increase in [Ca²⁺](i) was significantly inhibited by pretreatment of platelets with R59949, while thapsigargin-induced increase in [Ca²⁺](i) was comparable in platelets with and without R59949 pretreatment. Thapsigargin-induced increase in [Ca²⁺](i) was markedly attenuated in the presence of SKF-96365. In the presence of SKF-96365, thrombin-induced increase in [Ca²⁺](i) was significantly attenuated, and additional treatment with R59949 caused a further decrease in [Ca²⁺](i) . Pretreatment of platelets with 1-butanol significantly attenuated thrombin-induced increase in [Ca²⁺](i) , while thrombin-induced increase in [Ca²⁺](i) was augmented in the presence of propranolol. mRNA expression of DGK-α and DGK-γ, which are known to be inhibited by R59949, in platelets was confirmed by RT-PCR analysis.

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Hemangiomas are common vascular birthmarks that usually present a predictable pattern of proliferation and ultimate involution. Most do not require any treatment. When intervention is clinically indicated, medical and surgical options exist. Historically, corticosteroids have been used and have been shown to slow or stop the growth of a majority of hemangiomas; however, growth concerns and infectious complications have complicated their use. In 2008, a letter to the editor in The New England Journal of Medicine described another serendipitous observation of the effect of the nonselective beta-blocker, propranolol, on hemangiomas in 9 cases. This finding has been expanded by the authors of this original observation as well as others.

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Concomitant movement disorders, such as dystonia, are common among patients with childhood-onset ET, which supports the concept that ET is a heterogeneous disorder. Treatment strategies used for adult patients with ET seem to be effective also for children with ET, although controlled therapeutic trials in this population of patients with ET are lacking.

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Intractable fever in cancer patients is problematic and the causes of this fever can be diverse. Paroxysmal persistent hyperthermia after sudden mental change or neurologic deficit can develop via autonomic dysregulation without infection or any other causes of fever. Paroxysmal hyperthermic autonomic dysregulation is a rare disease entity. It manifests as a form of paroxysmal hypertension, fever, tachycardia, tachypnea, pupillary dilation, agitation and extensor posturing after traumatic brain injury, hydrocephalus, brain hemorrhage or brain neoplasm. We recently experienced a case of paroxysmal hyperthermia following intracerebral hemorrhage along with brain neoplasm. Extensive fever workups failed to show an infectious or inflammatory source and/or hormonal abnormality. Empirical treatments with antibiotics, antipyretics, morphine, steroid and antiepileptic agents were also ineffective. However, Propranolol, a lipophilic beta-blocker, successfully controlled the fever and stabilized the patient. Fever in cancer patients is a common phenomenon, but a central origin should be considered when the fever is intractable. Propranolol is one of the most effective drugs for treating paroxysmal hyperthermia that is due to autonomic dysregulation.

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This study evaluated the safety and effects of propranolol as a premedication before cataract surgery and compared them with the usual combination doses of fentanyl and ketamine. Among all reffered patients to Feiz Hospital of Esfahan for cataract surgery, 122 patients between Mar to Sep 2010 were enrolled in this study and randomly allocated into one of the following equal groups: 40 mg propranolol, 2 hours before surgery and combination of 15 mg ketamine and 50 µg fentanyl l. 5 min before surgery. The ability to control of hemodynamic instabilities caused by stress and to gain patients satisfaction was compared between two groups. Also, the efficacy of each premedication to control of hemodynamic changes during surgery were evaluated and compared. No significant differences were seen in the patients satisfaction and controlling of stress induced hemodynamic changes between two groups (P>0.05). However, patients in ketamine + fentanyl group showed more nausea and less pain during and after surgery. Moreover, no significant adverse effects were reported during and after the surgery. Our results demonstrated that propranolol can be used safely as a premedication in cataract surgery in the comparable efficacy to ketamine plus fentanyl premedication.

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Given its improved safety profile compared with systemic corticosteroids, propranolol has become the mainstay treatment of infantile haemangioma (IH) worldwide. There is evidence, mainly from adult volunteer studies, that propranolol use is associated with central nervous system (CNS) effects. Impairment to short- and long-term memory, psychomotor function, sleep quality and mood with relatively low doses and durations of treatment have been reported. The exact magnitude of CNS effects resulting from propranolol use, especially in the early developmental stages and for prolonged periods of use, is not currently known. These effects may not be readily recognizable and require specialized assessment of cognitive function not routinely performed. Furthermore, there may be a delay between exposure and cognitive defects. The evidence to date provides a strong rationale to proceed with caution when prescribing propranolol for IH: treatment should be used only when indicated (in the presence of ulceration, impairment of a vital function or risk of permanent disfigurement) and for a limited duration, and the benefits of treatment should be weighed carefully against potential adverse events before treatment is initiated. This narrative review describes the evidence for an effect of propranolol use on CNS function from volunteer and patient studies, including IH.

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An investigation of the optimal acquisition parameters for quantitation was conducted for propranolol, reserpine, leucine enkephalin and neurotensin from mouse plasma samples. The lower limits of quantitation were demonstrated to be 1-3 nM while the quantitation linear dynamic range extends to four orders of magnitude. This level of performance is sufficient for most bioanalytical applications in drug discovery.

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The sorption of three polychlorinated biphenyls (PCBs) in single-solute and bi-solute systems in the presence of propranolol was studied on biochars at pyrolyzing temperatures of 200°C (BC200) and 700°C (BC700). Hydrophobicity and molecular planarity played a major role in PCB sorption onto BC200 and BC700, respectively. The steric hindrance caused by non-planarity made the strong specific sorption sites on BC700 less accessible to nonplanar PCBs. In bi-solute systems for BC200, propranolol monomers at an initial concentration (Cinit) of 0.8mg/L inhibited the sorption of PCB4 by competing for sorption sites. Propranolol at Cinit larger than 1.2mg/L could form hemimicelle structures on the biochar surface, providing a favorable phase for PCB4 partitioning, thereby increasing Koc up to 1.15 times. For BC700, propranolol prohibited PCB4 sorption mainly by pore-blocking, with the log Koc being reduced from 4.92 to 3.94. This study informs the application of biochar in mixture-contaminated environment.

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buy inderal 40 mg 2016-07-22

From these results, we concluded that nicotine-induced relaxation of the guinea pig gallbladder is not mediated by the release of noradrenaline, nitric oxide (NO), prostaglandins, or a related substance, or by the activation of potassium channels, or by the stimulation Buy Ketoconazole 2 Cream of nicotinic cholinoceptors. Further work is needed to determine the cellular mechanism(s) of action by which nicotine acts on gallbladder smooth muscle.

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Studies have shown that therapy with beta-blockers reduces mortality in patients with heart failure. However, there are no studies describing the effects of propranolol on the QT dispersion in this population. The objective of this study was to assess the electrophysiological Buy Brahmi Tablets Online profile, mainly QT dispersion, of patients with heart failure regularly using propranolol.

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This study evaluated the antihypertensive efficacy and tolerability of a chronotherapeutic formulation of propranolol designed for nighttime dosing (propranolol controlled release [CR]). A total of 434 patients with mild-to-moderate hypertension were randomized to placebo or to one of four doses of propranolol CR (80, 120, 160, or 640 mg/d). At baseline, the mean morning blood pressures were similar in each treatment group and averaged 152/101 mm Hg. After 8 weeks of treatment, morning diastolic blood pressure, the primary efficacy measurement, was significantly reduced from baseline in placebo (-6.98 mm Hg) and all propranolol groups (p<0.001). The decreases ranged from 10.1 mm Hg in the 80-mg/d group to 11.0 mm Hg in the 120-mg/d group and were significantly larger than placebo in the 120-, 160-, and 640-mg/d groups (p<0.05). Blood pressure measured in the evening (trough) demonstrated similar antihypertensive efficacy. Heart rate and rate-pressure product were reduced in a dose-related manner by propranolol CR. The formulation was well tolerated with only fatigue and dizziness being reported more frequently than in the placebo group. Propranolol CR is an effective antihypertensive formulation that may reduce blood pressure Buy Ibuprofen India during the morning period of maximum cardiovascular risk.

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Eight children (age range: 1 day to 10 years) were diagnosed to have tachycardia-related ventricular dysfunction in the past 6 years. They presented with symptoms of palpitation, dyspnea and/or generalized swelling over the body of 3 months to 2 years'duration. The cardiothoracic ratio at presentation Buy Voltaren Emulgel Australia was 64% (52%-70%) and ejection fraction was 22.2% (15%-45%). In 7 patients tachycardia was diagnosed to be ectopic atrial and in 1 it was permanent junctional reciprocating tachycardia. Six of these children were managed with intravenous/oral amiodarone in combination with digoxin (3) and/or propranolol (2). In one child addition of amiodarone to digoxin and propranolol led to polymorphic ventricular tachycardia, and amiodarone was withdrawn. Only one child underwent radiofrequency ablation as the first choice because regular follow-up was not possible due to logistic reasons. Sinus rhythm with normalization of ventricular function was achieved in 6 of the 7 children treated medically. One child continued to have frequent episodes of tachycardia and underwent successful radiofrequency ablation of a high right atrial ectopic focus. Two out of the 6 patients on amiodarone could be managed with only digoxin and propranolol after their ventricular function had returned to normal. A third patient relapsed on stopping amiodarone and underwent successful radiofrequency ablation of a left atrial ectopic tachycardia.

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Tracheal rings from male adult Wistar rats were isolated and mounted in an organ bath containing Krebs-Henseleit solution under 1.5 g resting tension Buy Neem Leaf and contractions were recorded isometrically. After equilibrium period (60 min), cumulative concentrations of NaHS (0.2-1.2 mM) were applied on the tracheal basal tone or on the plateau of contractions induced by KCl (60 mM) or carbachol (CCh, 0.55 μM) in the absence and presence of certain antagonists and inhibitors.

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It is unclear if reduced hepatic drug elimination in congestive heart failure is primarily due to impairment of enzyme function as a result of tissue hypoxia, to the direct effects of hepatic congestion, or to changes intrinsic to the liver, such as reductions in enzyme content and activity Buy Real Cialis Online . We therefore compared propranolol clearance in perfused rat livers from animals with right ventricular failure (RVF) with that from control animals. Despite the fact that both groups were perfused at comparable flow rates, perfusion pressures, and levels of oxygen delivery, hepatic extraction of propranolol was significantly reduced in RVF livers (0.688 +/- 0.122 versus 0.991 +/- 0.006 ml/min/g of liver in controls, P <.001). This effect was reflected in a 97% reduction in propranolol intrinsic clearance in RVF livers (5 +/- 4 versus 172 +/- 82 ml/min/g of liver in controls, P <.01). In RVF livers, total hepatic CYP expression was reduced by 19% compared with controls, whereas cytochrome P450 isoenzymes 1A1/2 and 2D1 were reduced by 41 and 26%, respectively. Despite the 97% reduction in propranolol intrinsic clearance in perfused RVF liver, intrinsic clearance in microsomal preparations from the same livers was reduced by only 48% compared with controls (P <.05). These findings suggest that impaired propranolol clearance in RVF is not primarily accounted for by reduced hepatic oxygen delivery or by changes in hepatic content and activity of drug-metabolizing enzymes.

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We studied the effects of β-adrenoceptor antagonists propranolol and nadolol and L-type Ca(2+)-channel blocker verapamil on cardiac reperfusion injury developed after 45-min coronary occlusion. The substances were injected intravenously 5 min before reperfusion. The results indicate that activation of β-adrenoceptors Buy Neem Tree Online and opening of L-type Ca(2+)-channels promote the development of cardiac reperfusion injury, while blockage of β-adrenoceptors and/or L-type Ca(2+)-channels prevents reoxygenation-induced myocardial injury. Propranolol, nadolol, and verapamil can produce infraction-limiting effects after onset of ischemic heart injury.

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Epulis is a relapsable lesion in Buy Clarithromycin 500mg Tablets gingiva without specific treatment for its unexplained pathogenesis. Nowadays, surgical excision is the most popular method of treatment. To prevent recurrence, it is necessary to resect diseased tissues thoroughly, and even to remove the involved teeth. However, this may cause functional and cosmetic deformities. Therefore, it is urgent to find a new therapy without severe side effects. Infantile hemangioma is a common benign pediatric tumor which shares many features with epulis, such as rich vascularity, high incidence of female patients, high hormone level and similar treatments. A recent study showed that propranolol, a beta adrenergic receptor (β-AR) antagonist, was effective as treatment for infantile hemangioma. Our preliminary work showed that mRNA and protein levels of β2-AR were higher in epulis than in adjacent tissue. Therefore, we hypothesize that intralesional injection of propranolol may be useful as epulis treatment. Further work need to be done to confirm the safety and therapeutic effect of the treatment. After that, this specific β2-AR antagonist may be the first choice for epulis treatment.