The Effects of Airblast on Discriminated Avoidance Behavior in Rhesus Monkeys

Bogo, Victor; Hutton, Rebekah; Bruner, Alfred

doi:10.21236/ad0742819

Cited by 7 publications

(7 citation statements)

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“…48,88 This evidence is seen when comparing recent pulmonary fatality criteria of Bass 7 with the limited isolatedhead experiments of Krohn 59 and Clemedson 31 and the primary behavioral experiments of Bogo 11 (Fig. 2).…”

Section: Fundamental Questionsmentioning

confidence: 73%

“…These limited investigations suggested that pulmonary lethality occurred at much lower blast levels than brain fatalities, 31,59 and that, for very long-duration blasts, there are only transient behavioral consequences in primates at blast intensities that produce up to 50% pulmonary fatalities. 11 Owing to injury concerns, nuclear weapons establishments in the US and other countries developed detailed, orientation-dependent, injury assessments for pulmonary consequences of blast in terms of blast characteristics such as peak pressure and positivephase duration. 13 These have been recently revised with only large animal experiments for short-duration blasts, typically from high explosives.…”

Section: Injury Biomechanics and Injury Criteriamentioning

confidence: 99%

“…89 Close-ended shock tubes are capped at the end of the driven section, producing a stronger reflected shock wave back into the shock tube when the initial (incident) shock wave reaches the end of the driven section. 11 the shock tube mouth and an expansion wave propagates back into the tube beginning at the perimeter. Testing a specimen within a closed-ended shock tube ensures that the applied incident shock wave is a onedimensional plane wave.…”

Section: Shock Tube Testingmentioning

confidence: 99%

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Brain Injuries from Blast

et al. 2011

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Traumatic brain injury (TBI) from blast produces a number of conundrums. This review focuses on five fundamental questions including: (1) What are the physical correlates for blast TBI in humans? (2) Why is there limited evidence of traditional pulmonary injury from blast in current military field epidemiology? (3) What are the primary blast brain injury mechanisms in humans? (4) If TBI can present with clinical symptoms similar to those of Post-Traumatic Stress Disorder (PTSD), how do we clinically differentiate blast TBI from PTSD and other psychiatric conditions? (5) How do we scale experimental animal models to human response? The preponderance of the evidence from a combination of clinical practice and experimental models suggests that blast TBI from direct blast exposure occurs on the modern battlefield. Progress has been made in establishing injury risk functions in terms of blast overpressure time histories, and there is strong experimental evidence in animal models that mild brain injuries occur at blast intensities that are similar to the pulmonary injury threshold. Enhanced thoracic protection from ballistic protective body armor likely plays a role in the occurrence of blast TBI by preventing lung injuries at blast intensities that could cause TBI. Principal areas of uncertainty include the need for a more comprehensive injury assessment for mild blast injuries in humans, an improved understanding of blast TBI pathophysiology of blast TBI in animal models and humans, the relationship between clinical manifestations of PTSD and mild TBI from blunt or blast trauma including possible synergistic effects, and scaling between animals models and human exposure to blasts in wartime and terrorist attacks. Experimental methodologies, including location of the animal model relative to the shock or blast source, should be carefully designed to provide a realistic blast experiment with conditions comparable to blasts on humans. If traditional blast scaling is appropriate between species, many reported rodent blast TBI experiments using air shock tubes have blast overpressure conditions that are similar to human long-duration nuclear blasts, not high explosive blasts.

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Section: Fundamental Questionsmentioning

confidence: 73%

Section: Injury Biomechanics and Injury Criteriamentioning

confidence: 99%

Section: Shock Tube Testingmentioning

confidence: 99%

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Brain Injuries from Blast

et al. 2011

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“…Rhesus monkeys exposed to approximately 207 kPa (30 psi), 276 kPa (40 psi), or 345 kPa (50 psi) had significant, albeit transient, memory and performance deficits (Bogo et al , 1971). Considerable and persistent memory deficits have been shown for rats subjected to moderate- and low-intensity blast waves generated in an air-driven shock tube (Cernak et al , 2001 a ; Long et al , 2009 a ; Saljo et al , 2008).…”

Section: Primary Bintmentioning

confidence: 99%

Traumatic Brain Injury: An Overview of Pathobiology with Emphasis on Military Populations

Černak

Noble-Haeusslein

2009

J Cereb Blood Flow Metab

368

220

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This review considers the pathobiology of non-impact blast-induced neurotrauma (BINT). The pathobiology of traumatic brain injury (TBI) has been historically studied in experimental models mimicking features seen in the civilian population. These brain injuries are characterized by primary damage to both gray and white matter and subsequent evolution of secondary pathogenic events at the cellular, biochemical, and molecular levels, which collectively mediate widespread neuro-degeneration. An emerging field of research addresses brain injuries related to the military, in particular blast-induced brain injuries. What is clear from the effort to date is that the pathobiology of military TBIs, particularly BINT, has characteristics not seen in other types of brain injury, despite similar secondary injury cascades. The pathobiology of primary BINT is extremely complex. It comprises systemic, local, and cerebral responses interacting and often occurring in parallel. Activation of the autonomous nervous system, sudden pressure-increase in vital organs such as lungs and liver, and activation of neuroendocrine-immune system are among the most important mechanisms significantly contributing to molecular changes and cascading injury mechanisms in the brain.

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“…Reactive gliosis, neuronal swelling, and cytoplasmic vacuolation have also been observed in the hippocampus of rats subjected to thoracic blast injury (Cernak et al 2001). Rhesus monkeys exposed to high BOP (207 kPa, 276 kPa, or 345 kPa) demonstrated significant, albeit transient, memory and performance deficits (Bogo et al, 1971). …”

Section: Introductionmentioning

confidence: 99%

Increase in blood–brain barrier permeability, oxidative stress, and activated microglia in a rat model of blast‐induced traumatic brain injury

Readnower

Chavko

Adeeb

et al. 2010

J of Neuroscience Research

247

229

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Traumatic brain injury (TBI) as a consequence of exposure to blast is increasingly prevalent in military populations, with the underlying pathophysiological mechanisms mostly unknown. In the present study, we utilized an air-driven shock tube to investigate the effects of blast exposure (120 kPa) on rat brains. Immediately following exposure to blast neurological function was reduced. BBB permeability was measured using IgG antibody and evaluating its immunoreactivity in the brain. At 3 and 24 h post-exposure there was a transient significant increase in IgG staining in the cortex. At 3 days post-exposure IgG immunoreactivity returned to control levels. Quantitative immunostaining was employed to determine the temporal course of brain oxidative stress following exposure to blast. Levels of 4-hydroxynonenal (4HNE) and 3-nitrotyrosine (3NT) were significantly increased at 3 h post-exposure and returned to control levels at 24 h post-exposure. The response of microglia to blast exposure was determined by autoradiographic localization of 3 H-PK11195 binding. At 5 days post-exposure increased binding was observed in the contralateral and ipsilateral dentate gyrus. These regions also displayed increased binding at 10 days post-exposure; in addition to these regions there was increased binding in the contralateral ventral hippocampus and substantia nigra at this time point. Using antibodies against CD11b/c, microglia morphology characteristic of activated microglia was observed in the hippocampus and substantia nigra of animals exposed to blast. These results indicate that BBB breakdown, oxidative stress, and microglia activation likely play a role in the neuropathology associated with TBI as a result of blast exposure.

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The Effects of Airblast on Discriminated Avoidance Behavior in Rhesus Monkeys

Cited by 7 publications

References 0 publications

Brain Injuries from Blast

Brain Injuries from Blast

Traumatic Brain Injury: An Overview of Pathobiology with Emphasis on Military Populations

Increase in blood–brain barrier permeability, oxidative stress, and activated microglia in a rat model of blast‐induced traumatic brain injury

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