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functional and structural changes in the basilar artery due to overpressure blast injury.

Title: The functional and structural changes in the basilar artery due to overpressure blast injury.
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Name(s): Toklu, Hale Z, author
Muller-Delp, Judy, author
Yang, Zhihui, author
Oktay, Şehkar, author
Sakarya, Yasemin, author
Strang, Kevin, author
Ghosh, Payal, author
Delp, Michael D, author
Scarpace, Philip J, author
Wang, Kevin K W, author
Tümer, Nihal, author
Type of Resource: text
Genre: Journal Article
Text
Date Issued: 2015-12-01
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: Overpressure blast-wave induced brain injury (OBI) leads to progressive pathophysiologic changes resulting in a reduction in brain blood flow, blood brain barrier breakdown, edema, and cerebral ischemia. The aim of this study was to evaluate cerebral vascular function after single and repeated OBI. Male Sprague-Dawley rats were divided into three groups: Control (Naive), single OBI (30 psi peak pressure, 1 to 2 msec duration), and repeated (days 1, 4, and 7) OBI (r-OBI). Rats were killed 24 hours after injury and the basilar artery was isolated, cannulated, and pressurized (90 cm H2O). Vascular responses to potassium chloride (KCl) (30 to 100 mmol/L), endothelin-1 (10(-12) to 10(-7) mol/L), acetylcholine (ACh) (10(-10) to 10(-4) mol/L) and diethylamine-NONO-ate (DEA-NONO-ate) (10(-10) to 10(-4) mol/L) were evaluated. The OBI resulted in an increase in the contractile responses to endothelin and a decrease in the relaxant responses to ACh in both single and r-OBI groups. However, impaired DEA-NONO-ate-induced vasodilation and increased wall thickness to lumen ratio were observed only in the r-OBI group. The endothelin-1 type A (ET(A)) receptor and endothelial nitric oxide synthase (eNOS) immunoreactivity were significantly enhanced by OBI. These findings indicate that both single and r-OBI impairs cerebral vascular endothelium-dependent dilation, potentially a consequence of endothelial dysfunction and/or vascular remodelling in basilar arteries after OBI.
Identifier: FSU_pmch_26104291 (IID), 10.1038/jcbfm.2015.151 (DOI), PMC4671114 (PMCID), 26104291 (RID), 26104291 (EID), jcbfm2015151 (PII)
Grant Number: P30 AG028740
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4671114.
Subject(s): Animals
Basilar Artery/pathology
Blast Injuries/pathology
Brain Injuries/pathology
Capillaries/pathology
Male
Muscle Contraction/drug effects
Muscle, Smooth, Vascular/drug effects
Nitric Oxide Synthase Type III/drug effects
Nitric Oxide Synthase Type III/metabolism
Pressure
Rats
Rats, Sprague-Dawley
Receptor, Endothelin A/drug effects
Receptor, Endothelin A/metabolism
Vasoconstrictor Agents/pharmacology
Vasodilator Agents/pharmacology
Persistent Link to This Record: http://purl.flvc.org/fsu/fd/FSU_pmch_26104291
Owner Institution: FSU
Is Part Of: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
1559-7016
Issue: iss. 12, vol. 35

Choose the citation style.
Toklu, H. Z., Muller-Delp, J., Yang, Z., Oktay, Ş., Sakarya, Y., Strang, K., … Tümer, N. (2015). The functional and structural changes in the basilar artery due to overpressure blast injury. Journal Of Cerebral Blood Flow And Metabolism : Official Journal Of The International Society Of Cerebral Blood Flow And Metabolism. Retrieved from http://purl.flvc.org/fsu/fd/FSU_pmch_26104291