N-acetylcysteine Amide Ameliorates Blast-Induced Changes in Blood-Brain Barrier Integrity in Rats.

Traumatic brain injury resulting from exposure to blast overpressure (BOP) is associated with neuropathology including impairment of the blood-brain barrier (BBB). This study examined the effects of repeated exposure to primary BOP and post-blast treatment with an antioxidant, N-acetylcysteine amide (NACA) on the integrity of BBB. Anesthetized rats were exposed to three 110 kPa BOPs separated by 0.

Low-Level Primary Blast Induces Neuroinflammation and Neurodegeneration in Rats.

Objective: Mild blast traumatic brain injury is commonly prevalent in modern combat casualty care and has been associated with the development of neurodegenerative conditions. However, whether primary lower level blast overpressure (LBOP) causes neurodegeneration and neuroinflammation remains largely unknown. The aim of our present study was to determine whether LBOP can cause neuroinflammation and neurodegeneration.

Complement inhibition ameliorates blast-induced acute lung injury in rats: Potential role of complement in intracellular HMGB1-mediated inflammation.

Background And Objective: Complement activation as an early and important inflammatory process contributes to multiple organ dysfunction after trauma. We have recently shown that complement inhibition by decay-accelerating factor (DAF) protects brain from blast-overpressure (BOP)-induced damage. This study was conducted to determine the effect of DAF on acute lung injury induced by BOP exposure and to elucidate its possible mechanisms of action.

Protective Effect of -Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats.

Blast-induced traumatic brain injury is associated with acute and possibly chronic elevation of intracranial pressure (ICP). The outcome after TBI is dependent on the progression of complex processes which are mediated by oxidative stress. So far, no effective pharmacological protection against TBI exists.

Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume.

Blast-induced traumatic brain injury (bTBI) is a leading cause of injuries in recent military conflicts and it is responsible for an increased number of civilian casualties by terrorist attacks. bTBI includes a variety of neuropathological changes depending on the intensity of blast overpressure (BOP) such as brain edema, neuronal degeneration, diffuse axonal damage, and vascular dysfunction with neurological manifestations of psychological and cognitive abnormalities. Internal jugular vein (IJV) compression is known to reduce intracranial compliance by causing an increase in brain volume and was shown to reduce brain damage during closed impact-induced TBI.

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

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.

Advances in Intracranial Pressure Monitoring and Its Significance in Managing Traumatic Brain Injury.

Intracranial pressure (ICP) measurements are essential in evaluation and treatment of neurological disorders such as subarachnoid and intracerebral hemorrhage, ischemic stroke, hydrocephalus, meningitis/encephalitis, and traumatic brain injury (TBI). The techniques of ICP monitoring have evolved from invasive to non-invasive-with both limitations and advantages. Some limitations of the invasive methods include short-term monitoring, risk of infection, restricted mobility of the subject, etc.

Pathophysiology of blast-induced ocular trauma in rats after repeated exposure to low-level blast overpressure.

Background: The incidence of blast-induced ocular injury has dramatically increased due to advances in weaponry and military tactics. A single exposure to blast overpressure (BOP) has been shown to cause damage to the eye in animal models; however, on the battlefield, military personnel are exposed to BOP multiple times. The effects of repeated exposures to BOP on ocular tissues have not been investigated.

Pathophysiology of blast-induced ocular trauma with apoptosis in the retina and optic nerve.

Background: Blast-induced ocular trauma is a frequent cause of morbidity for survivors of improvised explosive devices. Blast overpressure (BOP) of 120 ± 7 KPa has been shown to cause damage to lungs, brain, and gut in a rat model; however, the effects of BOP on ocular tissues have not been characterized. To elucidate the pathophysiology of blast-induced ocular trauma, ocular tissues from rats subjected to blast were examined for evidence of apoptosis by the detection of activated caspase 3 and TUNEL assay in their ocular tissues.

Selective vulnerability of the cerebral vasculature to blast injury in a rat model of mild traumatic brain injury.

Background: Blast-related traumatic brain injury (TBI) is a common cause of injury in the military operations in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. The aim of the present study was to examine whether blast exposure affects the cerebral vasculature in a rodent model.

Telemetric intracranial pressure monitoring in blast-induced traumatic brain injury.

The long-term monitoring of intracranial pressure (ICP) is important for the management of acute and chronic neuropathological conditions which include head injury, traumatic brain injury, hydrocephalus, etc. In this study, we developed an implantable device for measuring ICP over long periods of time in an animal model of blast-induced brain injury. The performance of the device was first evaluated in vitro and subsequently utilized to measure ICP in rats exposed to blast overpressures.

Protective effects of decay-accelerating factor on blast-induced neurotrauma in rats.

Background: Blast-induced neurotrauma (BINT) is the signature life threatening injury of current military casualties. Neuroinflammation is a key pathological occurrence of secondary injury contributing to brain damage after blast injury. We have recently demonstrated that blast-triggered complement activation and cytokine release are associated with BINT.

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury.

Background: Blast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves affect the brain is poorly understood. To understand their effects, we analyzed the brains of rats exposed to single or multiple (three) 74.

Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor α (TNFα) release in a rat brain.

Blast-induced neurotrauma (BINT) is a major medical concern yet its etiology is largely undefined. Complement activation may play a role in the development of secondary injury following traumatic brain injury; however, its role in BINT is still undefined. The present study was designed to characterize the complement system and adaptive immune-inflammatory responses in a rat model of moderate BINT.

Assessment of the effects of acute and repeated exposure to blast overpressure in rodents: toward a greater understanding of blast and the potential ramifications for injury in humans exposed to blast.

Mild traumatic brain injury (mTBI) resulting from exposure to improvised explosive devices (IEDs) has fueled a requirement to develop animals models that mirror this condition using exposure to blast overpressure (BOP). En route to developing a model of repeated exposure to BOP we sought to initially characterize the effects of acute BOP exposure in rodents, focusing specifically on the levels of BOP exposure that produced clinical mTBI symptoms. We first measured BOP effects on gross motor function on a balance beam.

MicroRNA let-7i is a promising serum biomarker for blast-induced traumatic brain injury.

Blast-induced traumatic brain injury (TBI) is of significant concern in soldiers returning from the current conflicts in Iraq and Afghanistan. Incidents of TBI have increased significantly in the current conflicts compared to previous wars, and a majority of these injuries are caused by improvised explosive devices. Currently, no specific technique or biomarker is available for diagnosing TBI when no obvious clinical symptoms are present.

Blast-induced color change in photonic crystals corresponds with brain pathology.

A high incidence of blast exposure is a 21st century reality in counter-insurgency warfare. However, thresholds for closed-head blast-induced traumatic brain injury (bTBI) remain unknown. Moreover, without objective information about relative blast exposure, warfighters with bTBI may not receive appropriate medical care and may remain in harm's way.

Relationship between orientation to a blast and pressure wave propagation inside the rat brain.

Exposure to a blast wave generated during an explosion may result in brain damage and related neurological impairments. Several mechanisms by which the primary blast wave can damage the brain have been proposed, including: (1) a direct effect of the shock wave on the brain causing tissue damage by skull flexure and propagation of stress and shear forces; and (2) an indirect transfer of kinetic energy from the blast, through large blood vessels and cerebrospinal fluid (CSF), to the central nervous system. To address a basic question related to the mechanisms of blast brain injury, pressure was measured inside the brains of rats exposed to a low level of blast (~35kPa), while positioned in three different orientations with respect to the primary blast wave; head facing blast, right side exposed to blast and head facing away from blast.

Attenuation of pulmonary inflammation after exposure to blast overpressure by N-acetylcysteine amide.

Lung contusion is a common problem from blunt chest trauma caused by mechanical forces and by exposure to blast overpressure, often with fatal consequences. Lung contusion is also a risk factor for the development of pneumonia, severe clinical acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Infiltrating neutrophils are considered to be central mediators of lung injuries after blunt trauma.

Microarray analysis of gene expression in rat cortical neurons exposed to hyperbaric air and oxygen.

To gain a global view of the genomic response of neurons to normobaric and hyperbaric hyperoxic stress, we performed a microarray analysis of gene expression after exposure to varying levels of partial oxygen pressures. Rat neurons were exposed to normobaric hyperoxia, hyperbaric (2, 4, and 6 atmosphere absolute) air or hyperbaric O(2). We identified 183 genes significantly altered (increased or decreased >or=1.

Protection against blast-induced mortality in rats by hemin.

Background: A critical immediate determinant of survival after exposure to blast overpressure (BOP) is cardiovascular and respiratory impairment related to disruption of the alveolar septa and pulmonary capillaries and resulting in acute pulmonary hemorrhage. Hemoglobin (Hb) released from red cells can contribute to lethality by activation of oxidative stress reactions and severe vasoconstriction associated with hypoperfusion in the pulmonary microcirculation. Heme oxygenase-1 (HO-1) is activated by hemin, a product of Hb degradation and may confer protection against hemoglobin-mediated oxidative cell and tissue damage.

Mechanisms of protection against pulmonary hyperbaric O(2) toxicity by intermittent air breaks.

Intermittent exposure to air is used as a protective strategy against hyperbaric O(2) (HBO(2)) toxicity. Little is known about optimal intermittent exposure schedules and the mechanism of protection. In this study, we examined the role of antioxidant enzymes, and inflammatory cytokines in the mechanism of HBO(2) tolerance by intermittent air breaks.

Protein carbonyls as a biomarker of foetal-neonatal hypoxic stress.

Objectives: Investigation of the effect of hypoxic conditions during labour on the protein oxidative modifications and changes in plasma antioxidative capacity of newborns.

Design And Methods: Oxidative damage to proteins was determined by high-performance liquid chromatography. Antioxidative status was monitored by Trolox equivalent antioxidant capacity method.

Lung injury and recovery after exposure to blast overpressure.

Background: A critical immediate determinant of survival after exposure to blast overpressure (BOP) is pulmonary damage, but mechanisms of injury and the course of recovery are not well understood. The objective of this study was to characterize the progression of oxidative and inflammatory responses in lungs as well as the activation of consequent protective mechanisms after exposure to medium intensity BOP.

Methods: Rats were exposed to a moderate (approximately 120 kPa) level of BOP in a pneumatically driven shock tube.