Evidence map›Paper›PMID 26024446›Full record

ArticlePloS one2015

Blast-Associated Shock Waves Result in Increased Brain Vascular Leakage and Elevated ROS Levels in a Rat Model of Traumatic Brain Injury.

Shushi Kabu, Hayder Jaffer, Marianne Petro, Dave Dudzinski, Desiree Stewart, Amy Courtney, Michael Courtney, Vinod Labhasetwar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 69 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Shushi KabuLerner Research Institute, Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States of America.
Hayder JafferLerner Research Institute, Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States of America.
Marianne PetroLerner Research Institute, Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States of America.
Dave DudzinskiLerner Research Institute, Medical Device Solutions, Cleveland Clinic, Cleveland, Ohio, United States of America.
Desiree StewartLerner Research Institute, Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States of America.
Amy CourtneyBTG Research, Colorado Springs, Colorado, United States of America.
Michael CourtneyBTG Research, Colorado Springs, Colorado, United States of America.
Vinod LabhasetwarLerner Research Institute, Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States of America.
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blast-associated shock wave-induced traumatic brain injury (bTBI) remains a persistent risk for armed forces worldwide, yet its detailed pathophysiology remains to be fully investigated. In this study, we have designed and characterized a laboratory-scale shock tube to develop a rodent model of bTBI. Our blast tube, driven by a mixture of oxygen and acetylene, effectively generates blast overpressures of 20-130 psi, with pressure-time profiles similar to those of free-field blast waves. We tested our shock tube for brain injury response to various blast wave conditions in rats. The results show that blast waves cause diffuse vascular brain damage, as determined using a sensitive optical imaging method based on the fluorescence signal of Evans Blue dye extravasation developed in our laboratory. Vascular leakage increased with increasing blast overpressures and mapping of the brain slices for optical signal intensity indicated nonhomogeneous damage to the cerebral vasculature. We confirmed vascular leakage due to disruption in the blood-brain barrier (BBB) integrity following blast exposure. Reactive oxygen species (ROS) levels in the brain also increased with increasing blast pressures and with time post-blast wave exposure. Immunohistochemical analysis of the brain sections analyzed at different time points post blast exposure demonstrated astrocytosis and cell apoptosis, confirming sustained neuronal injury response. The main advantages of our shock-tube design are minimal jet effect and no requirement for specialized equipment or facilities, and effectively generate blast-associated shock waves that are relevant to battle-field conditions. Overall data suggest that increased oxidative stress and BBB disruption could be the crucial factors in the propagation and spread of neuronal degeneration following blast injury. Further studies are required to determine the interplay between increased ROS activity and BBB disruption to develop effective therapeutic strategies that can prevent the resulting cascade of neurodegeneration.

Indexed as

AnimalsBlast InjuriesBlood-Brain BarrierBlood VesselsBrainBrain EdemaBrain InjuriesDisease Models, AnimalEquipment DesignMaleRats, Sprague-DawleyReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID26024446
PMCPMC4449023
OpenAlexW1529163965

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.