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1

J, Delic, e Great Britain. Health and Safety Executive., eds. Propranolol: Criteria document for an occupational exposure limit. Sudbury: HSE Books, 1995.

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2

Paradiso, Frances Lori. The central nervous system effects and pharmacokinetics of propranolol enantiomers. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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3

Angrini, Manar A. Effect of propranolol and other 5-HT antagonists of motivated and emotional behaviour. [S.l: The Author], 1997.

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4

Hassounah, Ahmed. The effect of propranolol on renal prostaglandin-E2, the reninangiotensin and kidney function in rabbit. Salford: University of Salford, 1990.

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5

Mathieu, Charlotte. Phase III-Studie zur Wirksamkeit und Sicherheit von oralem Propranolol bei Säuglingen mit schweren, proliferierenden Hämangiomen. [S.l: s.n.], 2013.

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6

Pett, Burkhard. Der Einfluss von Propranolol auf die Dosiswirkungskurven der kardiovaskulären Effekte von Isoprenalin in Abhängigkeit von der dosis- und zeitabhängigen Besetzung von [beta]₁- und [beta]₂-Adrenozeptoren. [s.l.]: [s.n.], 1987.

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7

Hansen, Matthias. Monotherapie der Hyperthyreose mit R-Propranolol. 1995.

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8

Pitschner, Heinz-Friedrich. Zeitwirkungsverlauf und Plasmakonzentrationskinetik von Propranolol und Carteolol beim Menschen. 1986.

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9

Graf, Kai-Ivo. Einfluss von Propranolol auf [beta]₂-adrenerge Rezeptorendichten und -funktion. 1995.

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10

Puljevic, Mislav. Propranolol: Medical Uses, Mechanisms of Action and Potential Adverse Effects. Nova Science Publishers, Incorporated, 2015.

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11

Kampschulte, Hans-Jörg. Der Einfluss von Propranolol und Rifampicin auf die Pharmakokinetik von Phenprocoumon. 1993.

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12

Panton, Lynn B. Effect of aerobic exercise training on estimated hepatic blood flow and plasma propranolol concentration after oral administration in young and elderly adults. 1993.

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13

Publications, ICON Health. Propranolol - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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14

Metabolic response to acute cold air exposure and two levels of beta blockade in males and females. 1991.

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15

Saunders, Mike. Infantile capillary haemangiomas. Editado por John Phillips e Sally Erskine. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834281.003.0080.

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This chapter discusses Léauté-Labrèze, Dumas de la Roque, Hubiche, Boralevi, Thambo, and Taïeb’s paper on propranolol for severe haemangiomas of infancy including the design of the study (outcome measures, results, conclusions, and a critique).
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16

Bohmeyer, Susanne. Simultane Stimulation der Wachstumshormon- und Cortisolsekretion mit Nacom[trademark] udn Propranolol bei minderwüchsigen Kindern. 1995.

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17

Laxy, Thomas. Gegenüberstellung inhalativer Methacholin- und Propranolol-Provokationstests zum Nachweis der bronchialen Hyperreagibilität mit vorausgehendem Bodyplethysmographengerätevergleich. 1993.

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18

Quinton, S. D. Evaluation of propranolol for the prevention of postoperative arrhythmias in patients undergoing noncardiac thoracic surgery. 1994.

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19

Eggers, Rainer. Unspezifisch negativ inotrope wirkungen von acebutolol und bupranolol im vergleich zu propranolol unter berücksichtigung therapeutischer dosen. 1988.

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20

Kern, Klaus Hermann. Einfluss von Phentolamin, Propranolol, Atropin und Carbachol auf die Konzentration des Androgenrezeptors in der ventralen Rattenprostata. 1990.

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21

The effects of propranolol on carbohydrate and free fatty acids metabolism during maximal contraction in isolated canine gracilis muscle. 1986.

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22

The effects of propranolol on carbohydrate and free fatty acids metabolism during maximal contraction in isolated canine gracilis muscle. 1986.

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23

The effects of propranolol on carbohydrate and free fatty acids metabolism during maximal contraction in isolated canine gracilis muscle. 1985.

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24

Potempa, Kathleen Marie. A COMPARISON OF EXERCISE PERFORMANCE AND FATIGUE IN HYPERTENSIVE MEN OVER 50 YEARS OF AGE TAKING PROPRANOLOL AND PINDOLOL. 1986.

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25

The effects of propranolol on carbohydrate and free fatty acids metabolism during maximal contraction in isolated canine gracilis muscle. 1986.

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26

Dalvi, Arif, Kelly E. Lyons e Rajesh Pahwa. Essential Tremor. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0009.

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Essential tremor (ET) is the most common cause of tremor. Most studies suggest that the cerebellum is involved in the pathophysiology of ET and that it is an autosomal dominant disorder; however, the actual cause and a gene responsible for the majority of cases have not been identified. The diagnosis of ET is based on evaluation of clinical signs and symptoms. Pharmacological treatment is effective in 30% to 50% of casesm, with primidone and propranolol being first line therapies. Some benefit has also been reported with gabapentin, topiramate, and benzodiazepines. Deep brain stimulation effectively reduces medication-resistant ET in appropriate cases.
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27

The effects of selective and non-selective beta adrenoreceptor blockade on the cardiovascular system during isometric (static) exercise. 1988.

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28

The effects of selective and non-selective beta adrenoreceptor blockade on the cardiovascular system during isometric (static) exercise. 1988.

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29

Conviser, Jason M. The effects of selective and non-selective beta adrenoreceptor blockade on the cardiovascular system during isometric (static) exercise. 1988.

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30

Conviser, Jason M. The effects of selective and non-selective beta adrenoreceptor blockade on the cardiovascular system during isometric (static) exercise. 1987.

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31

Stammeier, Raimund. Studie über die antiischämische Wirksamkeit der Kombination von Mononitrat und Propranolol im Vergleich zu ihren Einzelsubstanzen bei Patienten mit koronarer Herzkrankheit. 1992.

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32

Cen, Jianping. Modulation of cytokine profiles in HaCaT keratinocytes and human fibroblasts by lithium, propranolol, and chloroquine as known trigger factors for psoriasis. 2006.

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33

Raberg, Rainer. Die isolierte feldgereizte Meerschweinchentrachea: Wirkung von Peptiden (Bradykinin, Substanz P, Angiotensin II) und anderen Pharmaka (Atropin, Propranolol, Tetrodotoxin, Dipyridamol, 4-Aminopyridin). 1985.

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34

Mey, Christian de. Untersuchungen zu den pharmakodynamischen und pharmakokinetischen Eigenschaften sowie zur Verträglichkeit nach einmaliger und wiederholter transdermaler Applikation der [beta]-Adrenozeptorblocker Propranolol und Mepindolol beim Menschen. 1990.

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35

Use of Propranolol for Stress the Long View Your 21st Psychiatric Consultation William R. Yee M. D. , J. D. , Copyright Applied for Jan. 30 2021. Lulu Press, Inc., 2023.

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36

Schwartz, Peter J., e Lia Crotti. Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—catecholaminergic polymorphic ventricular tachycardia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0152.

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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited disorder associated with syncope and sudden death manifesting in the young during sympathetic activation. The electrocardiogram is normal and the heart is structurally normal. The diagnosis is usually made with an exercise stress test that shows a typical pattern of onset and offset of adrenergically induced ventricular arrhythmias. Molecular screening of RyR2, the major CPVT gene, is recommended whenever the suspicion of CPVT is high. If a disease-causing mutation is identified, cascade screening allows pre-symptomatic diagnosis among family members. All affected subjects should be treated with beta blockers (nadolol or propranolol). Preliminary data support the association of beta blockers with flecainide. After a cardiac arrest, an implantable cardioverter defibrillator (ICD) should be implanted, but it is accompanied by a disquietingly high incidence of adverse effects. After syncope on beta blocker therapy, left cardiac sympathetic denervation is most effective, preserves quality of life, and does not preclude a subsequent ICD implantation.
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37

Isbister, Geoffrey, e Colin Page. Management of β‎-blocker and calcium channel blocker poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0325.

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β‎-blocker and calcium channel-blockers can cause life-threatening toxicity due to cardiogenic shock. Both β‎-blockers and calcium channel-blockers are heterogenous groups of drugs and particular drugs, such as propranolol, diltiazem, and verapamil are far more toxic than the others in their class. The most important investigations in β‎-blocker and calcium channel-blocker overdose are an electrocardiogram, blood glucose measurement, and electrolytes. Like most overdoses, supportive treatment is the most important, with emphasis on the primary pathophysiology. Early decontamination should be considered based on the severity of the poisoning. Treatment of β‎-blockers and calcium channel-blockers poisoning, using absolute blood pressure as an endpoint can be misleading and measuring cardiac output can be more informative in gauging response to treatment. There are no specific antidotes, although β‎-agonists may be effective in β‎-blocker overdose and calcium has been shown to be effective in calcium channel-blocker overdose. The choice of inotropes and/or vasopressors will differ for β‎-blockers and calcium channel-blockers. These include isoprenaline, high dose insulin euglycaemia, phosphodiesterase inhibitors, and other catecholaminergic inotropes for β‎-blocker poisoning and adrenaline, high dose insulin euglycaemia and vasopressors for calcium channel-blocker poisoning.
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