Protective Effect of N-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...
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doaj-f780ae0dc4fc4c55aae16840d543fae92020-11-25T01:08:11ZengFrontiers Media S.A.Frontiers in Neurology1664-22952017-06-01810.3389/fneur.2017.00219259849Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in RatsUsmah Kawoos0Richard M. McCarron1Richard M. McCarron2Mikulas Chavko3Department of Neurotrauma, Naval Medical Research Center, Silver Spring, MD, United StatesDepartment of Neurotrauma, Naval Medical Research Center, Silver Spring, MD, United StatesDepartment of Surgery, Uniformed Services University of the Health Sciences, Walter Reed National Military Medical Center, Bethesda, MD, United StatesDepartment of Neurotrauma, Naval Medical Research Center, Silver Spring, MD, United StatesBlast-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. In this study, rats were exposed to a single or repetitive blast overpressure (BOP) at moderate intensities of 72 or 110 kPa in a compressed air-driven shock tube. The degree and duration of the increase in ICP were proportional to the intensity and frequency of the blast exposure(s). In most cases, a single dose of antioxidant N-acetylcysteine amide (NACA) (500 mg/kg) administered intravenously 2 h after exposure to BOP significantly attenuated blast-induced increase in ICP. A single dose of NACA was not effective in improving the outcome in the group of animals that were subjected to repetitive blast exposures at 110 kPa on the same day. In this group, two treatments with NACA at 2 and 4 h post-BOP exposure resulted in significant attenuation of elevated ICP. Treatment with NACA prior to BOP exposure completely prevented the elevation of ICP. The findings indicate that oxidative stress plays an important role in blast-induced elevated ICP as treatment with NACA-ameliorated ICP increase, which is frequently related to poor functional recovery after TBI.http://journal.frontiersin.org/article/10.3389/fneur.2017.00219/fullblast overpressuretraumatic brain injuryintracranial pressureoxidative stressN-acetylcysteine amide |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Usmah Kawoos Richard M. McCarron Richard M. McCarron Mikulas Chavko |
spellingShingle |
Usmah Kawoos Richard M. McCarron Richard M. McCarron Mikulas Chavko Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats Frontiers in Neurology blast overpressure traumatic brain injury intracranial pressure oxidative stress N-acetylcysteine amide |
author_facet |
Usmah Kawoos Richard M. McCarron Richard M. McCarron Mikulas Chavko |
author_sort |
Usmah Kawoos |
title |
Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats |
title_short |
Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats |
title_full |
Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats |
title_fullStr |
Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats |
title_full_unstemmed |
Protective Effect of N-Acetylcysteine Amide on Blast-Induced Increase in Intracranial Pressure in Rats |
title_sort |
protective effect of n-acetylcysteine amide on blast-induced increase in intracranial pressure in rats |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Neurology |
issn |
1664-2295 |
publishDate |
2017-06-01 |
description |
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. In this study, rats were exposed to a single or repetitive blast overpressure (BOP) at moderate intensities of 72 or 110 kPa in a compressed air-driven shock tube. The degree and duration of the increase in ICP were proportional to the intensity and frequency of the blast exposure(s). In most cases, a single dose of antioxidant N-acetylcysteine amide (NACA) (500 mg/kg) administered intravenously 2 h after exposure to BOP significantly attenuated blast-induced increase in ICP. A single dose of NACA was not effective in improving the outcome in the group of animals that were subjected to repetitive blast exposures at 110 kPa on the same day. In this group, two treatments with NACA at 2 and 4 h post-BOP exposure resulted in significant attenuation of elevated ICP. Treatment with NACA prior to BOP exposure completely prevented the elevation of ICP. The findings indicate that oxidative stress plays an important role in blast-induced elevated ICP as treatment with NACA-ameliorated ICP increase, which is frequently related to poor functional recovery after TBI. |
topic |
blast overpressure traumatic brain injury intracranial pressure oxidative stress N-acetylcysteine amide |
url |
http://journal.frontiersin.org/article/10.3389/fneur.2017.00219/full |
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