Abstract | BACKGROUND:
Traumatic brain injury causes a disruption of the vascular endothelial glycocalyx layer that is associated with an overactivation of the sympathoadrenal system. We hypothesized that early and unselective beta-blockade with propranolol alone or in combination with the alfa2-agonist clonidine would decrease brain edema, blood-brain barrier permeability, and glycocalyx disruption at 24 hours after trauma. METHODS: We subjected 53 adult male Sprague-Dawley rats to lateral fluid percussion brain injury and randomized infusion with propranolol (n = 16), propranolol + clonidine (n = 16), vehicle (n = 16), or sham (n = 5) for 24 hours. Primary outcome was brain water content at 24 hours. Secondary outcomes were blood-brain barrier permeability and plasma levels of syndecan-1 (glycocalyx disruption), cell damage ( histone-complexed DNA fragments), epinephrine, norepinephrine, and animal motor function. RESULTS: CONCLUSION:
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Authors | Gustav Folmer Genét, Peter Bentzer, Morten Bagge Hansen, Sisse Rye Ostrowski, Pär Ingemar Johansson |
Journal | The journal of trauma and acute care surgery
(J Trauma Acute Care Surg)
Vol. 84
Issue 1
Pg. 89-96
(01 2018)
ISSN: 2163-0763 [Electronic] United States |
PMID | 28930945
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Adrenergic alpha-2 Receptor Agonists
- Adrenergic beta-Antagonists
- Propranolol
- Clonidine
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Topics |
- Adrenergic alpha-2 Receptor Agonists
(pharmacology)
- Adrenergic beta-Antagonists
(pharmacology)
- Animals
- Blood-Brain Barrier
(drug effects)
- Brain Edema
(etiology, metabolism, pathology)
- Brain Injuries, Traumatic
(complications, metabolism, pathology)
- Capillary Permeability
(drug effects)
- Clonidine
(pharmacology)
- Disease Models, Animal
- Glycocalyx
(drug effects, metabolism, pathology)
- Male
- Propranolol
(pharmacology)
- Rats
- Rats, Sprague-Dawley
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