Blast Exposure in Rats with Body Shielding Is Characterized Primarily by Diffuse Axonal Injury
| Autor: | Edwin K. Jackson, Patrick M. Kochanek, Richard A. Bauman, David V. Ritzel, Hülya Bayır, Steven Parks, Robert S. B. Clark, Peter V. Swauger, Valerian E. Kagan, Lawrence C. Tong, Larry W. Jenkins, Robert C. Switzer, Robert H. Garman, C. Edward Dixon |
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| Rok vydání: | 2011 |
| Předmět: |
Male
Pathology medicine.medical_specialty Traumatic brain injury H&E stain Poison control Diffuse Axonal Injury Rats Sprague-Dawley Protective Clothing Blast Injuries medicine Animals Pounds per square inch Blast wave business.industry Diffuse axonal injury Brain Apnea Hypothermia medicine.disease Axons Rats Disease Models Animal Neurology (clinical) medicine.symptom business |
| Zdroj: | Journal of Neurotrauma. 28:947-959 |
| ISSN: | 1557-9042 0897-7151 |
| Popis: | Blast-induced traumatic brain injury (TBI) is the signature insult in combat casualty care. Survival with neurological damage from otherwise lethal blast exposures has become possible with body armor use. We characterized the neuropathologic alterations produced by a single blast exposure in rats using a helium-driven shock tube to generate a nominal exposure of 35 pounds per square inch (PSI) (positive phase duration ∼ 4 msec). Using an IACUC-approved protocol, isoflurane-anesthetized rats were placed in a steel wedge (to shield the body) 7 feet inside the end of the tube. The left side faced the blast wave (with head-only exposure); the wedge apex focused a Mach stem onto the rat's head. The insult produced ∼ 25% mortality (due to impact apnea). Surviving and sham rats were perfusion-fixed at 24 h, 72 h, or 2 weeks post-blast. Neuropathologic evaluations were performed utilizing hematoxylin and eosin, amino cupric silver, and a variety of immunohistochemical stains for amyloid precursor protein (APP), glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba1), ED1, and rat IgG. Multifocal axonal degeneration, as evidenced by staining with amino cupric silver, was present in all blast-exposed rats at all time points. Deep cerebellar and brainstem white matter tracts were most heavily stained with amino cupric silver, with the morphologic staining patterns suggesting a process of diffuse axonal injury. Silver-stained sections revealed mild multifocal neuronal death at 24 h and 72 h. GFAP, ED1, and Iba1 staining were not prominently increased, although small numbers of reactive microglia were seen within areas of neuronal death. Increased blood-brain barrier permeability (as measured by IgG staining) was seen at 24 h and primarily affected the contralateral cortex. Axonal injury was the most prominent feature during the initial 2 weeks following blast exposure, although degeneration of other neuronal processes was also present. Strikingly, silver staining revealed otherwise undetected abnormalities, and therefore represents a recommended outcome measure in future studies of blast TBI. |
| Databáze: | OpenAIRE |
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