Mechanisms and pathophysiology of the low-level blast brain injury in animal models

Säljö, Annette; Mayorga, Maria; Bolouri, Hayde; Svensson, Berndt; Hamberger, Anders

doi:10.1016/j.neuroimage.2010.05.050

Cited by 66 publications

(39 citation statements)

References 34 publications

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“…Animals exposed to howitzer blasts at 30 kPa although displayed parenchymal and subarachnoid hemorrhages, they were not significantly different from that of controls due to the limitations in the number of animals. Säljö et al concluded that low levels of blast causes brain edema as indicated by increased bioelectric impedance, an increase in intracranial pressure, small brain hemorrhages and impaired cognitive function [49]. In our study the animals were exposed to higher open field blast pressure than these animals and the likelihood of such hemorrhages although possible was not investigated as the focus was to study neuronal injury and glial reactivity changes.…”

Section: Discussionmentioning

confidence: 94%

Neuronal Injury and Glial Changes Are Hallmarks of Open Field Blast Exposure in Swine Frontal Lobe

Kallakuri

Desai

et al. 2017

PLoS ONE

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With the rapid increase in the number of blast induced traumatic brain injuries and associated neuropsychological consequences in veterans returning from the operations in Iraq and Afghanistan, the need to better understand the neuropathological sequelae following exposure to an open field blast exposure is still critical. Although a large body of experimental studies have attempted to address these pathological changes using shock tube models of blast injury, studies directed at understanding changes in a gyrencephalic brain exposed to a true open field blast are limited and thus forms the focus of this study. Anesthetized, male Yucatan swine were subjected to forward facing medium blast overpressure (peak side on overpressure 224–332 kPa; n = 7) or high blast overpressure (peak side on overpressure 350–403 kPa; n = 5) by detonating 3.6 kg of composition-4 charge. Sham animals (n = 5) were subjected to all the conditions without blast exposure. After a 3-day survival period, the brain was harvested and sections from the frontal lobes were processed for histological assessment of neuronal injury and glial reactivity changes. Significant neuronal injury in the form of beta amyloid precursor protein immunoreactive zones in the gray and white matter was observed in the frontal lobe sections from both the blast exposure groups. A significant increase in the number of astrocytes and microglia was also observed in the blast exposed sections compared to sham sections. We postulate that the observed acute injury changes may progress to chronic periods after blast and may contribute to short and long-term neuronal degeneration and glial mediated inflammation.

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Section: Discussionmentioning

confidence: 94%

Neuronal Injury and Glial Changes Are Hallmarks of Open Field Blast Exposure in Swine Frontal Lobe

Kallakuri

Desai

et al. 2017

PLoS ONE

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“…Time-course of ICP changes in groups of rats exposed to low-level blasts were reported by Saljo et al [22]. Under low levels of single blast exposure, ICP showed a slow-rising, sustained increase to a maximum level, following which it gradually declined to the normal levels [22]. Saljo et al reported a dependence of increase in ICP (peak and delay in elevation) on the intensity of blast when rats were exposed to a single blast of 10, 30, and 60 kPa [21].…”

Section: Introductionmentioning

confidence: 88%

“…Interestingly the transient increase in ICP during exposure to a blast wave (138 kPa) generated in shock tube had a higher magnitude than the blast wave itself [19]. Time-course of ICP changes in groups of rats exposed to low-level blasts were reported by Saljo et al [22]. Under low levels of single blast exposure, ICP showed a slow-rising, sustained increase to a maximum level, following which it gradually declined to the normal levels [22].…”

Section: Introductionmentioning

confidence: 99%

Effects of Exposure to Blast Overpressure on Intracranial Pressure and Blood-Brain Barrier Permeability in a Rat Model

Kawoos

Lankasky

et al. 2016

PLoS ONE

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Exposure to blast overpressure (BOP) activates a cascade of pathological processes including changes in intracranial pressure (ICP) and blood-brain barrier (BBB) permeability resulting in traumatic brain injury (TBI). In this study the effect of single and multiple exposures at two intensities of BOP on changes in ICP and BBB permeability in Sprague-Dawley rats was evaluated. Animals were exposed to a single or three repetitive (separated by 0.5 h) BOPs at 72 kPa or 110 kPa. ICP was monitored continuously via telemetry for 6 days after exposure to BOP. The alteration in the permeability of BBB was determined by extravasation of Evans Blue (EB) into brain parenchyma. A significant increase in ICP was observed in all groups except the single 72 kPa BOP group. At the same time a marked increase in BBB permeability was also seen in various parts of the brain. The extent of ICP increase as well as BBB permeability change was dependent on intensity and frequency of blast.

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“…Various species have been examined including: rodents (Kaur et al, 1995, 1997), nonhuman primates (Lu et al, 2012), and pigs (Bauman et al, 2009; de Lanerolle et al, 2011). To complement these efforts, in-laboratory blast testing has been performed using shock tubes, which are typically cylindrical tubes where rats (Cernak et al, 2001a, b; Saljo et al, 2001, 2002a, b, 2011; Long et al, 2009; Readnower et al, 2010; Cullen et al, 2011; Garman et al, 2011; Park et al, 2011), mice (Cernak et al, 2011; Koliatsos et al, 2011), and ferrets (Rafaels et al, 2012) have been exposed to blast-like pressure wave propagation driven by compressed gas (e.g., air, nitrogen, helium). Other studies have employed explosive charge-driven shock tubes (Saljo et al, 2000; Reneer et al, 2011).…”

Section: Animal Model Of Blast-induced Traumatic Brain Injurymentioning

confidence: 99%

Animal models of traumatic brain injury

Johnson

Meaney

Cullen

et al. 2015

Handbook of Clinical Neurology

131

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Mechanisms and pathophysiology of the low-level blast brain injury in animal models

Cited by 66 publications

References 34 publications

Neuronal Injury and Glial Changes Are Hallmarks of Open Field Blast Exposure in Swine Frontal Lobe

Neuronal Injury and Glial Changes Are Hallmarks of Open Field Blast Exposure in Swine Frontal Lobe

Effects of Exposure to Blast Overpressure on Intracranial Pressure and Blood-Brain Barrier Permeability in a Rat Model

Animal models of traumatic brain injury

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