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Drug and Therapeutics Bulletin Nov 1975
Topics: Humans; Migraine Disorders; Propranolol
PubMed: 1192946
DOI: No ID Found -
Clinical Pharmacology and Therapeutics 1968
Topics: Animals; Dogs; Guinea Pigs; Humans; Intestinal Absorption; Mice; Propranolol; Rabbits; Rats
PubMed: 5676807
DOI: 10.1002/cpt196895696 -
Journal of Psychiatry & Neuroscience :... 2022Reconsolidation impairment using propranolol is a novel intervention for mental disorders with an emotional memory at their core. In this systematic review and... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Reconsolidation impairment using propranolol is a novel intervention for mental disorders with an emotional memory at their core. In this systematic review and meta-analysis, we examined the evidence for this intervention in healthy and clinical adult samples.
METHODS
We searched 8 databases for randomized, double-blind studies that involved at least 1 propranolol group and 1 placebo group. We conducted a meta-analysis of 14 studies ( = 478) in healthy adults and 12 studies in clinical samples ( = 446).
RESULTS
Compared to placebo, reconsolidation impairment under propranolol resulted in reduced recall of aversive material and cue-elicited conditioned emotional responses in healthy adults, as evidenced by an effect size (Hedges ) of -0.51 ( = 0.002, 2-tailed). Moreover, compared to placebo, reconsolidation impairment under propranolol alleviated psychiatric symptoms and reduced cue-elicited reactivity in clinical samples with posttraumatic stress disorder, addiction or phobia ( = -0.42, = 0.010).
LIMITATIONS
Methodological differences between studies posed an obstacle for identifying sources of heterogeneity.
CONCLUSION
Reconsolidation impairment is a robust, well-replicated phenomenon in humans. Its clinical use is promising and deserves further controlled investigation.
Topics: Adrenergic beta-Antagonists; Adult; Emotions; Humans; Mental Recall; Propranolol; Randomized Controlled Trials as Topic
PubMed: 35361699
DOI: 10.1503/jpn.210057 -
British Medical Journal Jun 1974Beta-blocking drugs that prevent cranial vasodilatation are potentially valuable in the prophylaxis of migraine. Forty-nine patients with either classic or common... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
Beta-blocking drugs that prevent cranial vasodilatation are potentially valuable in the prophylaxis of migraine. Forty-nine patients with either classic or common migraine were treated with propranolol 160 mg/day for an average of six months. The first 30 of the patients to respond well to this treatment then participated in a double-blind cross-over trial with a placebo and propranolol. The mean frequency of headache attacks was significantly reduced by propranolol. None of the patients expressed a preference for placebo. Propranolol seems to be an effective prophylactic for common and classic migraine but the antimigraine properties of the various beta-blocking agents probably differ.
Topics: Clinical Trials as Topic; Female; Humans; Male; Migraine Disorders; Placebos; Propranolol; Respiration; Respiratory Tract Diseases
PubMed: 4604977
DOI: 10.1136/bmj.2.5921.699 -
Tremor and Other Hyperkinetic Movements... 2024Essential tremor, the world's most prevalent movement disorder, lacks a clear understanding of its pathophysiology. Propranolol, a non-specific beta-blocker capable of...
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.
Topics: Humans; Propranolol; Essential Tremor; Motor Cortex; Movement; Tremor
PubMed: 38189055
DOI: 10.5334/tohm.829 -
The New England Journal of Medicine Sep 1977
Topics: Humans; Propranolol; Thyroid Crisis
PubMed: 895777
DOI: 10.1056/nejm197709222971222 -
Neurobiology of Learning and Memory Mar 2018The therapeutic efficacy of the synthetic β-adrenergic receptor blocker, propranolol, for the treatment of post-traumatic stress disorder (PTSD) is currently being...
The therapeutic efficacy of the synthetic β-adrenergic receptor blocker, propranolol, for the treatment of post-traumatic stress disorder (PTSD) is currently being debated. Mixed results have been published regarding propranolol's ability to disrupt the consolidation and reconsolidation of memories. Here, we use the invertebrate model Lymnaea to study propranolol's ability to disrupt consolidation of memories formed under varying various types of stress which cause differing degrees of emotional memory. We show that when propranolol is administered immediately following operant conditioning, only the consolidation process of memories enhanced by individual stressors (i.e. a non-emotional memory) is susceptible to disruption. However, when propranolol is administered prior to training, only memories enhanced by a combination of stressors leading to an emotional memory are susceptible to disruption. These data suggest that the time of propranolol administration, as well as the type of memory formed play a key role in propranolol's ability to obstruct memory consolidation.
Topics: Adrenergic beta-Antagonists; Animals; Emotions; Lymnaea; Memory Consolidation; Propranolol; Stress, Physiological
PubMed: 29412170
DOI: 10.1016/j.nlm.2018.01.010 -
Lancet (London, England) Nov 1985
Clinical Trial
Topics: Biological Availability; Dosage Forms; Humans; Male; Propranolol
PubMed: 2865633
DOI: 10.1016/s0140-6736(85)92701-1 -
Annals of Plastic Surgery Sep 2014Infantile hemangiomas (IHs) are the most common tumor of infancy, yet there are no Food and Drug Administration-approved therapeutics to date. Recently, the nonselective...
BACKGROUND
Infantile hemangiomas (IHs) are the most common tumor of infancy, yet there are no Food and Drug Administration-approved therapeutics to date. Recently, the nonselective β-adrenergic-blocker propranolol has been shown to be a safe and effective means of treating IHs, although its mechanism has yet to be elucidated. We have previously demonstrated that propranolol induces early and incomplete adipogenesis in stem cells derived from hemangiomas. We hypothesize that propranolol promotes dysregulated adipogenesis via the improper regulation of adipogenic genes.
METHODS
Hemangioma stem cells (HemSCs) isolated from resected IH specimens were treated with adipogenic medium for 1 or 4 days in either propranolol or vehicle. Cell death was measured by the incorporation of annexin V and propidium iodide by flow cytometry. Adipogenesis was assessed by visualizing lipid droplet formation by Oil Red O staining. Proadipogenic genes C/EBPα, C/EBPβ, C/EBPδ, PPARδ, PPARγ, RXRα, and RXRγ were analyzed by quantitative reverse transcription and polymerase chain reaction.
RESULTS
Hemangioma stem cells treated with propranolol increased lipid droplet formation compared to vehicle-treated cells indicating increased adipogenesis. Cell death as measured by FACS analysis indicated that the propranolol-treated cells died due to necrosis and not apoptosis. During adipogenesis, transcript levels of PPARδ, PPARγ, C/EBPβ, and C/EBPδ were significantly increased (P<0.01) in propranolol-treated cells relative to control cells. In contrast, RXRα and RXRγ levels were significantly decreased (P<0.05), and C/EBPα, a gene required for terminal adipocyte differentiation, was strongly suppressed by propranolol when compared to vehicle-treated cells (P<0.01).
CONCLUSIONS
In HemSCs, propranolol accelerated dysregulated adipogenic differentiation characterized by improper adipogenic gene expression. Consistent with accelerated adipogenesis, propranolol significantly increased the expression of the proadipogenic genes, PPARγ, C/EBPβ, and C/EBPγ compared to control. However, propranolol treatment also led to improper induction of PPARδ and suppression of C/EBPα, RXRα, and RXRγ. Taken together these data indicate that propranolol promoted dysregulated adipogenesis and inhibited the HemSCs from becoming functional adipocytes, ultimately resulting in cell death. Understanding this mechanism behind propranolol's effectiveness will be a vital factor in producing more effective therapies in the future.
Topics: Adipogenesis; Hemangioma; Humans; Neoplastic Stem Cells; Propranolol; Time Factors; Tumor Cells, Cultured
PubMed: 25115372
DOI: 10.1097/SAP.0000000000000272 -
Journal of Ocular Pharmacology and... Mar 2021Propranolol, a nonselective B1/B2 adrenoceptor antagonist, promotes the regression of infantile hemangiomas likely through suppression of vascular endothelial growth...
Propranolol, a nonselective B1/B2 adrenoceptor antagonist, promotes the regression of infantile hemangiomas likely through suppression of vascular endothelial growth factor (VEGF), which prompted its use for the prevention of retinopathy of prematurity. We tested the hypothesis that topical ocular propranolol is safe and effective for reducing the severity of oxygen-induced retinopathy (OIR) in the neonatal rat intermittent hypoxia (IH) model. At birth (P0), rat pups were randomly assigned to room air or neonatal intermittent hypoxia (IH) consisting of 50% O with brief episodes of hypoxia (12% O) from P0 to P14, during which they received a single daily dose of oral propranolol (1 mg/kg/day in 50 μL in sterile normal saline) or topical ocular propranolol (0.2% in 10 μL in normal saline) from P5 to P14. Placebo-controlled littermates received 50 μL oral or 10 μL topical ocular sterile normal saline. Retinal vascular and astrocyte integrity; retinal histopathology and morphometry; and angiogenesis biomarkers were determined. Topical ocular propranolol improved retinal vascular damage and preserved the astrocytic template, but did not completely prevent OIR. The beneficial effects of propranolol were associated with reduced ocular VEGF and increased endogenous soluble inhibitor, sVEGFR-1, when administered topically. Propranolol failed to completely prevent severe OIR, however, it prevented astrocyte degeneration resulting from neonatal IH-induced damage. We conclude that the mechanisms of propranolol's beneficial effects in neonatal IH may involve in part, astrocyte preservation.
Topics: Administration, Oral; Animals; Disease Models, Animal; Female; Humans; Infant, Newborn; Oxygen; Pregnancy; Propranolol; Rats; Rats, Sprague-Dawley; Retinopathy of Prematurity
PubMed: 33535016
DOI: 10.1089/jop.2020.0092