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Endothelin and the neurovascular unit in pediatric traumatic brain injury
Journal article   Open access   Peer reviewed

Endothelin and the neurovascular unit in pediatric traumatic brain injury

William M Armstead and Ramesh Raghupathi
Neurological research (New York), v 33(2), pp 127-132
Mar 2011
PMID: 21801587
url
https://europepmc.org/articles/pmc3545647View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Animals Animals, Newborn Brain Injuries - complications Brain Injuries - drug therapy Brain Injuries - physiopathology Cerebrovascular Disorders - drug therapy Cerebrovascular Disorders - etiology Cerebrovascular Disorders - physiopathology Child Disease Models, Animal Endothelin-1 - antagonists & inhibitors Endothelin-1 - cerebrospinal fluid Endothelin-1 - toxicity Female Hemodynamics - physiology Humans Male Nerve Degeneration - etiology Nerve Degeneration - metabolism Nerve Degeneration - pathology Sus scrofa
This study characterized the association between endothelin-1, cerebral hemodynamics, and histopathology after fluid percussion brain injury in the newborn pig. Lateral fluid percussion injury was induced in newborn pigs equipped with a closed cranial window. Cerebral blood flow was determined with radiolabeled microspheres and cerebrospinal fluid endothelin-1 was measured by radioimmunoassay. Cerebrospinal fluid endothelin-1 was increased from 26±4 to 296±37 pg/ml (∼10(-10) M) at 8 hours following fluid percussion injury. Post-injury treatment (30 minutes) with the endothelin-1 antagonist BQ-123 (1 mg/kg, intravenous) blocked pial artery vasoconstriction to topical endothelin-1 (∼10(-10) M) and blunted fluid percussion injury-induced reductions in cerebral blood flow at 8 hours post-insult (56±6 and 26±4 ml/minute versus 57±6 and 40± ml/minute; 100 g for cerebral blood flow before injury and 8 hours post-fluid percussion injury in vehicle and BQ-123 post-treated animals, respectively). Fluid percussion injury resulted in neuronal cell loss and decreased microtubule associated protein 2 immunoreactivity in the parietal cortex, which were blunted by BQ-123. These data indicate that fluid percussion injury-induced changes in cerebral hemodynamics are associated with neuronal damage and that endothelin-1 contributes to fluid percussion injury-induced histopathologic changes.

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33 citations in Scopus

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Collaboration types
Domestic collaboration
Web of Science research areas
Clinical Neurology
Neurosciences
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