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Journal articles on the topic 'Propranolol'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2024

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1

Kobeleva, Tatyana A., Alik I. Sichko, Marina I. Popova, and Elena M. Shapovalova. "Development and validation of a spectrophotometric method for the analysis of propranolol in a new soft dosage form "Propranozol"." Человек и его здоровье 24, no. 4 (2021): 83–90. http://dx.doi.org/10.21626/vestnik/2021-4/11.

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At present, the issue of creating and introducing into medical practice domestically produced drugs, the quality of man-ufacture of which is established using objective, highly sensitive optical physical and chemical methods, becomes relevant. Objective: to develop a spectrophotometric method for analysis of propranololol in the ointment "Propranozol" made on the basis of "Tizol" gel. Materials and methods. Pharmaceutical substance propranolol, gel "Tizol", soft dosage form "Propranosol" containing 0.5% of beta-adrenoblocker in titanium-containing base were used in the study. The analysis was carried out by spectropho-tometric method in the near ultraviolet region using a domestic device SF-2000. The method was validated according to State Pharmacopoeia of the Russian Federation, XIV edition, General Pharmacopeia Article 1.1.0012.15 "Validation of analytical methods". The developed method was validated according to the following metrological characteristics: specificity, linearity, reliability and precision. Statistical processing of the measurement results was performed according to the requirements of SPh RF XIV edition by methods of modern mathematical statistics (regression analysis), using a personal computer and MSOffice application package. Results. When studying propranolol absorption spectra in the ultraviolet region it was found that spectrophotometric analysis of this compound is rationally performed at a wavelength of 290 nm. The content of propranolol in the soft dosage form, found by the equation of the calibration graph, is within the range of 0.0470-0.0582 g, which corresponds to the allow-able standards of deviation given in the regulatory documentation. Conclusion. During the experimental study optimal conditions were chosen and the method of spectrophotometric quantitative determination of propranololol in the ointment "Propranozol" was developed with the relative error not exceed-ing ± 1.60 %.

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Li, Mi, and Yanqin Ji. "Propranolol Inhibits the Growth of Cervical Cancer Cells by Inhibiting Cyclic Guanosine Monophosphate/Protein Kinase G (cGMP/PKG) Pathway." Journal of Biomaterials and Tissue Engineering 12, no. 2 (February 1, 2022): 422–26. http://dx.doi.org/10.1166/jbt.2022.2916.

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This study assesses the therapeutic effect of propranolol on cervical cancer and its mechanism. Propranolol’s effect on cervical cancer was evaluated by MTT, Western blotting, flow cytometry and colony formation. By searching Drug Bank and String, cGMP/PKG signaling might be downstream targets of propranolol for subsequent analysis. Our results found that propranolol could significantly inhibit Hela and SiHA cell vitality and clone formation in a dose dependent manner. Further, Annexin V-PE/7-AAD Apoptosis Detection assay showed that propranolol could increase Hela and SiHA cell apoptosis. Finally, propranolol attenuated the phosphorylation level of VASP at Ser239 which is critical for PKG activation. In conclusion, propranolol suppressed cervical cancer cell proliferation via inhibition of cGMP/PKG signaling, which provides an affordable and effective method for cervical cancer remedy.

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Sowinski, Kevin M., and Brad S. Burlew. "Impact of CYP2D6 Poor Metabolizer Phenotype on Propranolol Pharmacokinetics and Response." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 17, no. 6 (November 12, 1997): 1305–10. http://dx.doi.org/10.1002/j.1875-9114.1997.tb03097.x.

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We conducted an open‐label study to determine the impact of cytochrome P‐4502D6 (CYP2D6) on propranolol pharmacokinetics and response in 12 healthy men with CYP2D6 extensive metabolizer (EM) phenotype and 3 healthy men with CYP2D6 poor metabolizer (PM) phenotype. Subjects received R,S‐propranolol hydrochloride 80 mg every 8 hours for 16 doses. After the sixteenth dose, blood and urine samples were collected for 24 hours, and serum propranolol and urine metabolite concentrations were determined by chiral high‐performance liquid chromatography. Heart rate response to treadmill exercise was measured serially over 24 hours. Apparent oral clearance of propranolol and partial metabolic clearance values of propranolol to 4‐hydroxypropranolol (HOP), propranolol glucuronide, and naphloxylactic acid (NLA) were estimated. Apparent oral clearance and elimination half‐life of propranolol were not different between EMs and PMs. Partial metabolic clearance of propranolol to HOP was significantly higher and to NLA was significantly lower in EMs than in PMs. No differences in percentage reductions in exercise heart rate were observed between EMs and PMs. The CYP2D6 PM phenotype has no effect on propranolol blood concentrations and does not alter response to propranolol. Our data also suggest that CYP2D6 mediates approximately 65% and 70% of S‐ and R‐propranolol's 4‐hydroxylation, respectively.

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Hurley, Elisa A. "Pharmacotherapy to Blunt Memories of Sexual Violence: What's a Feminist to Think?" Hypatia 25, no. 3 (2010): 527–52. http://dx.doi.org/10.1111/j.1527-2001.2010.01108.x.

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It has recently been discovered that propranolol—a beta-blocker traditionally used to treat cardiac arrhythmias and hypertension—might disrupt the formation of the emotionally disturbing memories that typically occur in the wake of traumatic events and consequently prevent the onset of trauma-induced psychological injuries such as Post-traumatic Stress Disorder. One context in which the use of propranolol is generating interest in both the popular and scientific press is sexual violence. Nevertheless, feminists have so far not weighed in on propranolol. I suggest that the time is ripe for a careful feminist analysis of the moral and political implications of propranolol use in the context of sexual violence. In this paper, I map the feminist issues potentially raised by providing propranolol to victims of sexual assault, focusing in particular on the compatibility of propranolol use and availability with an understanding of the social and systematic dimensions of rape's harms. I do not deliver a final verdict on propranolol; in fact, I show that we do not yet have enough information about propranolol's effects to do so. Rather, I provide a feminist framework for evaluating the possibilities and perils opened up by therapeutic memory manipulation in the context of sexual violence against women.

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Alotaibi, Hadil Faris, Haifa Alotaibi, Khaled M. Darwish, El-Sayed Khafagy, Amr S. Abu Lila, Mohamed A. M. Ali, Wael A. H. Hegazy, and Samar Zuhair Alshawwa. "The Anti-Virulence Activities of the Antihypertensive Drug Propranolol in Light of Its Anti-Quorum Sensing Effects against Pseudomonas aeruginosa and Serratia marcescens." Biomedicines 11, no. 12 (November 28, 2023): 3161. http://dx.doi.org/10.3390/biomedicines11123161.

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The development of bacterial resistance is an increasing global concern that requires discovering new antibacterial agents and strategies. Bacterial quorum sensing (QS) systems play important roles in controlling bacterial virulence, and their targeting could lead to diminishing bacterial pathogenesis. In this context, targeting QS systems without significant influence on bacterial growth is assumed as a promising strategy to overcome resistance development. This study aimed at evaluating the anti-QS and anti-virulence activities of the β-adrenoreceptor antagonist propranolol at sub-minimal inhibitory concentrations (sub-MIC) against two Gram-negative bacterial models Pseudomonas aeruginosa and Serratia marcescens. The effect of propranolol on the expression of QS-encoding genes was evaluated. Additionally, the affinity of propranolol to QS receptors was virtually attested. The influence of propranolol at sub-MIC on biofilm formation, motility, and production of virulent factors was conducted. The outcomes of the propranolol combination with different antibiotics were assessed. Finally, the in vivo protection assay in mice was performed to assess propranolol’s effect on lessening the bacterial pathogenesis. The current findings emphasized the significant ability of propranolol at sub-MIC to reduce the formation of biofilms, motility, and production of virulence factors. In addition, propranolol at sub-MIC decreased the capacity of tested bacteria to induce pathogenesis in mice. Furthermore, propranolol significantly downregulated the QS-encoding genes and showed significant affinity to QS receptors. Finally, propranolol at sub-MIC synergistically decreased the MICs of different antibiotics against tested bacteria. In conclusion, propranolol might serve as a plausible adjuvant therapy with antibiotics for the treatment of serious bacterial infections after further pharmacological and pharmaceutical studies.

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Kumar, Lalit, and Puneet Utreja. "Oleic Acid Vesicles for Transdermal Delivery of Propranolol Hydrochloride: Development and Characterization." Current Drug Therapy 15, no. 3 (October 14, 2020): 238–48. http://dx.doi.org/10.2174/1574885514666190722164119.

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Background: Pharmaceutical scientists are exploring transdermal route for treatment of various systemic diseases nowadays. Transdermal nanocarrier systems show various advantages like bioavailability enhancement of drugs, avoidance of first pass hepatic metabolism, and reduction of dosing frequency of bioactive therapeutic molecules. Objective: The objective of the present research work was to encapsulate Propranolol hydrochloride into oleic acid vesicles and carry out in-vitro and in-vivo evaluation of oleic acid vesicular gel containing Propranolol hydrochloride. Method: Propranol hydrochloride loaded oleic acid vesicles were prepared by exploring thin film hydration method. Developed vesicles were evaluated for morphology, size, zeta potential and polydispersity index (PDI). Thermal behavior of drug loaded vesicles was checked using differential scanning calorimetry (DSC) and depth of skin penetration was determined using confocal laser scanning microscopy (CLSM). Oleic acid vesicles dispersed in Carbopol 934R gel were subjected to in-vivo evaluation in male Sprague Dawley rats through measurement of plasma concentration and tissue distribution of Propranolol hydrochloride. Results: Optimized formulation having oleic acid : Propranol hydrochloride in the ratio 7 : 3 showed highest entrapment (56.1 ± 0.7%), acceptable size (291.3 ± 2.2 nm), the optimum value of PDI (0.219 ± 0.043) and zeta potential (-27.13 ± 0.25 mV). The results of DSC analysis showed effective encapsulation of drug inside the vesicles and CLSM analysis revealed penetration of vesicles upto stratum spinosum layer of skin. The results of in-vivo study revealed capability of vesicular gel to prolong the release of Propranolol hydrochloride upto 24 h with a Cmax value of 83.6 ± 3.0 ng/mL which was higher compared to the marketed tablet of Propranolol hydrochloride [InderalR (40 mg), Abbott India Ltd.] (45.6 ± 3.1 ng/mL). Tissue distribution studies revealed higher percentage of Propranolol hydrochloride in various organs after 24 h of administration of vesicular gel compared to marketed tablet. Conclusion: Developed oleic acid vesicular gel could be effective to reduce dosing frequency and avoid side effects of oral Propranol hydrochloride.

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Miguel-Puga, Adán, Gabriel Villafuerte, Mario Treviño, Emmanuel Ortega-Robles, and Oscar Arias-Carrión. "Effect of Propranolol on Motor Cortex Excitability in Essential Tremor: An Exploratory Study." Tremor and Other Hyperkinetic Movements 14 (January 2, 2024): 1. http://dx.doi.org/10.5334/tohm.829.

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Background: Essential tremor, the world’s most prevalent movement disorder, lacks a clear understanding of its pathophysiology. Propranolol, a non-specific beta-blocker capable of crossing the blood-brain barrier, is a primary choice for essential tremor treatment. While its tremor-reducing effects are generally attributed to peripheral actions, various uses hint at central adrenergic effects. Nevertheless, propranolol’s precise impact on the central nervous system in essential tremor subjects remains unexplored. Methods: In this study, we employed transcranial magnetic stimulation to assess the influence of propranolol on the excitability of the primary motor cortex (M1) in patients with essential tremor, compared to an age- and sex-matched control group. Cortical excitability parameters were measured following placebo and propranolol administration, encompassing resting and active motor thresholds, motor evoked potential characteristics, cortical silent period, and the input/output curve. Results: Distinct effects were observed across the two cortical hemispheres. Essential tremor patients displayed inhibition of the left M1 cortex and heightened excitability in the right M1 cortex four hours after propranolol administration, but not following placebo. Conclusions: These findings suggest potential differential noradrenergic excitatory and inhibitory modulation. However, comprehensive understanding necessitates further investigations, including left-handed participants and more diverse essential tremor subpopulations. This study underscores the need for continued exploration to unravel propranolol’s complex effects on motor cortex excitability in essential tremor.

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&NA;. "Propranolol see Maprotiline/propranolol." Reactions Weekly &NA;, no. 341 (March 1991): 10. http://dx.doi.org/10.2165/00128415-199103410-00057.

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Gulzar, G. M., Showkat A. Zargar, M. S. Alai, S. Jalal, Gul Javid, B. A. Khan, Pawan Suri, A. Shah, M. A. Khan, and Jaswinder Singh. "Effect of acute administration of propranolol, carvedilol, iso-sorbide dinitrate, “propranolol plus iso-sorbide dinitrate” and “carvedilol plus iso-sorbide dinitrate” on portal venus pressure." JMS SKIMS 16, no. 2 (December 12, 2013): 80–85. http://dx.doi.org/10.33883/jms.v16i2.215.

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Pharmacotherapy of portal hypertension in patients with cirrhosis includes beta-blockers, nitrates, somatastain analogues, alpha-blockers like prazocin. These drugs differ widely in their effectiveness, adverse effects and patient compliance. Beta-blockers particularly propranolol are the most commonly used drugs. Of late, carvedilol has been used and found to be superior to propranolol. The present study was aimed at assessing the effect of propranolol, carvedilol, iso-sorbide dinitrate; combination of “propranolol and iso-sorbide-dinitrate” and carvedilol and isosorbide dinitrate” on portal venous pressure in cirrhosis of liver. 40 consecutive patients with cirrhosis were subjected to hepatic venous catheterization. Baseline free and wedged hepatic venous pressures were recorded. Patients were randomly assigned to receive propranolol. 40 mgm PO (n=8); carvedilol 25mg PO (n=8); iso-sorbide dinitrate 20 mg PO (n-8); propranol plus iso-sorbide dinitrate (40 mg and 20 mg) (n=8) and carvedilol plus iso-sorbide dinitrate (25 mg and 20 mg PO) (n=8). Hemodynamic values were repeated 90 minutes after drug administration. All drugs significantly decreased the hepatic venous pressure gradient. Combination of carvedilol and iso-sorbide dinitrate was found to be most effective. The mean ± SD drop in hepatic venous pressure gradient was: propranolol 4.3 ± 1.4 mmHg (27%); Carvedilol 4.4 ± 1.8 mmHg (30%); iso-sorbide dinitrate 2.8 ± 1.4 mmHg (17%); propranolol plus iso-sorbide dinitrate” 5.1 ± 1.0 mmHg (31%) and “Carvedilol plus iso-sorbide dinitrate” 5.5 ± 1.2 mmHg (36%). Conclusion: combination of carvedilol and iso-sorbide dinitrate is the most effective anti-portal hypertensive regimen in patients of cirrhosis. JMS 2013;16(2):80-85

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10

Lucido, Christopher, W. Miskimins, and Paola Vermeer. "Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC." Cancers 10, no. 12 (November 30, 2018): 476. http://dx.doi.org/10.3390/cancers10120476.

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Tumor cell metabolism differs from that of normal cells, conferring tumors with metabolic advantages but affording opportunities for therapeutic intervention. Accordingly, metabolism-targeting therapies have shown promise. However, drugs targeting singular metabolic pathways display limited efficacy, in part due to the tumor’s ability to compensate by using other metabolic pathways to meet energy and growth demands. Thus, it is critical to identify novel combinations of metabolism-targeting drugs to improve therapeutic efficacy in the face of compensatory cellular response mechanisms. Our lab has previously identified that the anti-cancer activity of propranolol, a non-selective beta-blocker, is associated with inhibition of mitochondrial metabolism in head and neck squamous cell carcinoma (HNSCC). In response to propranolol, however, HNSCC exhibits heightened glycolytic activity, which may limit the effectiveness of propranolol as a single agent. Thus, we hypothesized that propranolol’s metabolic effects promote a state of enhanced glucose dependence, and that propranolol together with glycolytic inhibition would provide a highly effective therapeutic combination in HNSCC. Here, we show that glucose deprivation synergizes with propranolol for anti-cancer activity, and that the rational combination of propranolol and dichloroacetate (DCA), a clinically available glycolytic inhibitor, dramatically attenuates tumor cell metabolism and mTOR signaling, inhibits proliferation and colony formation, and induces apoptosis. This therapeutic combination displays efficacy in both human papillomavirus-positive (HPV(+)) and HPV(−) HNSCC cell lines, as well as a recurrent/metastatic model, while leaving normal tonsil epithelial cells relatively unaffected. Importantly, the combination significantly delays tumor growth in vivo with no evidence of toxicity. Additionally, the combination of propranolol and DCA enhances the effects of chemoradiation and sensitizes resistant cells to cisplatin and radiation. This novel therapeutic combination represents a promising treatment strategy which may overcome some of the limitations of targeting individual metabolic pathways in cancer.

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&NA;. "Propranolol see Butalbital/imipramine/propranolol." Reactions Weekly &NA;, no. 381 (December 1991): 10. http://dx.doi.org/10.2165/00128415-199103810-00050.

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&NA;. "Propranolol see Captopril/methyldopa/propranolol." Reactions Weekly &NA;, no. 305 (June 1990): 7. http://dx.doi.org/10.2165/00128415-199003050-00035.

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13

Tchivileva, Inna E., Richard Ohrbach, Roger B. Fillingim, Pei Feng Lim, Massimiliano Di Giosia, Margarete Ribeiro-Dasilva, John H. Campbell, et al. "Effect of comorbid migraine on propranolol efficacy for painful TMD in a randomized controlled trial." Cephalalgia 41, no. 7 (February 9, 2021): 839–50. http://dx.doi.org/10.1177/0333102421989268.

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Introduction The migraine-preventive drug propranolol is efficacious in reducing pain from temporomandibular disorder, suggesting potential modifying or mediating effects of comorbid migraine. Methods In this randomized controlled trial, myofascial temporomandibular disorder patients were treated with propranolol or placebo for 9 weeks. The primary endpoint was change in a facial pain index derived from daily symptom diaries. Linear and logistic regression models tested for a migraine × treatment-group interaction in reducing facial pain index. Counterfactual models explored changes in headache impact and heart rate as mediators of propranolol's efficacy. Results Propranolol's efficacy in reducing facial pain index was greater among the 104 migraineurs than the 95 non-migraineurs: For example, for the binary ≥ 30% reduction in facial pain index, odds ratios were 3.3 (95% confidence limits: 1.4, 8.1) versus 1.3 (0.5, 3.2), respectively, although the interaction was statistically non-significant ( p = 0.139). Cumulative response curves confirmed greater efficacy for migraineurs than non-migraineurs (differences in area under the curve 26% and 6%, respectively; p = 0.081). While 9% of the treatment effect was mediated by reduced headache impact, 46% was mediated by reduced heart rate. Conclusions Propranolol was more efficacious in reducing temporomandibular disorder pain among migraineurs than non-migraineurs, with more of the effect mediated by reduced heart rate than by reduced headache impact. Study identification and registration SOPPRANO; NCT02437383; https://clinicaltrials.gov/ct2/show/NCT02437383

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1377 (November 2011): 32–33. http://dx.doi.org/10.2165/00128415-201113770-00112.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1384 (January 2012): 48. http://dx.doi.org/10.2165/00128415-201213840-00190.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1389 (February 2012): 36–37. http://dx.doi.org/10.2165/00128415-201213890-00132.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 759 (July 1999): 10. http://dx.doi.org/10.2165/00128415-199907590-00029.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1171 (September 2007): 23. http://dx.doi.org/10.2165/00128415-200711710-00062.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1121 (September 2006): 20–21. http://dx.doi.org/10.2165/00128415-200611210-00065.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1356 (June 2011): 31. http://dx.doi.org/10.2165/00128415-201113560-00106.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1363 (August 2011): 34. http://dx.doi.org/10.2165/00128415-201113630-00136.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1363 (August 2011): 35. http://dx.doi.org/10.2165/00128415-201113630-00137.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1363 (August 2011): 35. http://dx.doi.org/10.2165/00128415-201113630-00140.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1363 (August 2011): 35. http://dx.doi.org/10.2165/00128415-201113630-00141.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1364 (August 2011): 38. http://dx.doi.org/10.2165/00128415-201113640-00148.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1366 (August 2011): 25–26. http://dx.doi.org/10.2165/00128415-201113660-00094.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1367 (September 2011): 32. http://dx.doi.org/10.2165/00128415-201113670-00112.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 562 (August 1995): 10. http://dx.doi.org/10.2165/00128415-199505620-00038.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 428 (November 1992): 11. http://dx.doi.org/10.2165/00128415-199204280-00053.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 432 (December 1992): 15. http://dx.doi.org/10.2165/00128415-199204320-00083.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 457 (June 1993): 12. http://dx.doi.org/10.2165/00128415-199304570-00048.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 458 (July 1993): 10. http://dx.doi.org/10.2165/00128415-199304580-00049.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 683 (January 1998): 11–12. http://dx.doi.org/10.2165/00128415-199806830-00031.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1400 (May 2012): 35. http://dx.doi.org/10.2165/00128415-201214000-00133.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1402 (May 2012): 38–39. http://dx.doi.org/10.2165/00128415-201214020-00142.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1408 (June 2012): 27. http://dx.doi.org/10.2165/00128415-201214080-00094.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1409 (July 2012): 38. http://dx.doi.org/10.2165/00128415-201214090-00125.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1415 (August 2012): 41–42. http://dx.doi.org/10.2165/00128415-201214150-00149.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1415 (August 2012): 42. http://dx.doi.org/10.2165/00128415-201214150-00151.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1416 (August 2012): 37. http://dx.doi.org/10.2165/00128415-201214160-00122.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 372 (October 1991): 8. http://dx.doi.org/10.2165/00128415-199103720-00044.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 403 (May 1992): 7. http://dx.doi.org/10.2165/00128415-199204030-00023.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 417 (September 1992): 10. http://dx.doi.org/10.2165/00128415-199204170-00041.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1111 (July 2006): 19. http://dx.doi.org/10.2165/00128415-200611110-00058.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1114 (August 2006): 16–17. http://dx.doi.org/10.2165/00128415-200611140-00047.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 924 (October 2002): 10. http://dx.doi.org/10.2165/00128415-200209240-00026.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1280 (November 2009): 39. http://dx.doi.org/10.2165/00128415-200912800-00133.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1283 (January 2010): 78–79. http://dx.doi.org/10.2165/00128415-201012830-00248.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1232 (December 2008): 28. http://dx.doi.org/10.2165/00128415-200812320-00083.

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&NA;. "Propranolol." Reactions Weekly &NA;, no. 1249 (April 2009): 38–39. http://dx.doi.org/10.2165/00128415-200912490-00119.

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