Beta blockers exposure and traumatic brain injury: a literature review

Tran, Tim; Dunne, Irie E; German, John W.

doi:10.3171/foc.2008.25.10.e8

Cited by 38 publications

(31 citation statements)

References 130 publications

(133 reference statements)

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“…The increased CMR in the injured brain, with defective autoregulation, can exacerbate the pre-existing ischemia and metabolic crisis following TBI (2). This hyperadrenergic state may contribute to increased mortality after TBI (3) and, conversely, patients with low levels of adrenergic stress as evidenced by a normal heart rate may have reduced mortality after TBI (4). …”

Section: Introductionmentioning

confidence: 99%

Beta-blockers and Traumatic Brain Injury

et al. 2017

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OBJECTIVE To determine if beta-(β)-blockers improve outcomes after acute traumatic brain injury (TBI). BACKGROUND There have been no new inpatient pharmacologic therapies to improve TBI outcomes in a half-century. Treatment of TBI patients with β-blockers offers a potentially beneficial approach. METHODS Using MEDLINE, EMBASE, and CENTRAL databases, eligible articles for our systematic review and meta-analysis (PROSPERO CRD42016048547) included adult (age≥16 years) blunt trauma patients admitted with TBI. The exposure of interest was β-blocker administration initiated during the hospitalization. Outcomes were mortality, functional measures, quality of life, cardiopulmonary morbidity (e.g. hypotension, bradycardia, bronchospasm, and/or congestive heart failure). Data were analyzed using a random-effects model, and represented by pooled odds ratio (OR) with 95% confidence intervals (CI) and statistical heterogeneity (I2). RESULTS Data were extracted from 9 included studies encompassing 2005 unique TBI patients with β-blocker treatment and 6240 unique controls. Exposure to β-blockers after TBI was associated with a reduction of in-hospital mortality (pooled OR 0.39, 95%CI: 0.27–0.56; I2=65%, p<0.00001). None of the included studies examined functional outcome or quality of life measures, and cardiopulmonary adverse events were rarely reported. No clear evidence of reporting bias was identified. CONCLUSIONS In adults with acute TBI, observational studies reveal a significant mortality advantage with β-blockers; however, quality of evidence is very low. We conditionally recommend the use of in-hospital β-blockers. However, we recommend further high-quality trials to answer questions about the mechanisms of action, effectiveness on subgroups, dose-response, length of therapy, functional outcome, and quality of life after β-blocker use for TBI.

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Section: Introductionmentioning

confidence: 99%

Beta-blockers and Traumatic Brain Injury

et al. 2017

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“…ANOVA with Bonferroni multiple comparison tests: Saline, P [ 0.05; Butoxamine: 0 versus 120 min: P \ 0.05* the neurotransmitter adrenaline. It has been known for decades that brain injury is associated with a significant catecholamine surge, and that adrenaline levels have been observed to increase several fold in patients with closed head injury [22]. Though a late surge of catecholamines may be detrimental [23], we proposed that the stress-related release of adrenaline may play an important role in brain neuroprotection by triggering a mechanism causing blood glutamate reduction.…”

Section: Discussionmentioning

confidence: 98%

The Activation of β2-Adrenergic Receptors in Naïve Rats Causes a Reduction of Blood Glutamate Levels: Relevance to Stress and Neuroprotection

et al. 2011

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This study examines the effects of the activation of β1 and β2-adrenergic receptors on glutamate homeostasis in the blood of naïve rats. Forty five male Sprague-Dawley rats were randomly assigned into one of seven treatment groups that were treated with various β-adrenergic receptor agonist and antagonist drugs. Blood glutamate levels were determined at t = 0, 30, 60, 90, and 120 min. The activation of β1 and β2-adrenergic receptors via isoproterenol hydrochloride administration produced a marked sustained decrease in blood glutamate levels by 60 min after treatment (ANOVA, t = 60, 90 min: P < 0.05, t = 120 min: P < 0.01). Pretreatment with propranolol hydrochloride (a non-selective β-adrenergic receptor blocker) or butaxamine hydrochloride (a selective β2-adrenergic receptor blocker) occluded the isoproterenol-mediated decrease in blood glutamate levels. Propranolol alone had no effect on blood glutamate levels. Selective β1-adrenergic receptor blockade with metoprolol resulted in decreased blood glutamate levels (ANOVA, t = 90 min: P < 0.05, t = 120 min: P < 0.01). Butaxamine hydrochloride alone resulted in a delayed-onset increase in glutamate levels (ANOVA, t = 120 min: P < 0.05). The results suggest that the activation of β2 receptors plays an important role in the homeostasis of glutamate in rat blood.

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“…catecholamine surge-associated pulmonary vascular permeability change leading to neurogenic pulmonary edema (7). This injury-induced excess of catecholamine also lends itself to hypertension, abnormal heart variability and neurological deficits (44,90,112). More recent clinical studies implicate the production and release of inflammatory mediators, including HMGB1 (8,49,75,122).…”

Section: Hmgb1 and Traumatic Brain Injurymentioning

confidence: 93%