Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury

Rim H. Al-Samsam, Beat Alessandri, Ross Bullock

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

We evaluated the acute changes in interstitial and whole brain N-acetyl- aspartate (NAA) measured by high-performance liquid chromatography in animal models of isolated traumatic brain injury (TBI) and TBI combined with secondary insult (hypotension-hypoxia [HH]). The Marmarou impact-acceleration model was used. Four groups were studied: (1) sham-operated control, (2) TBI alone (TBI 500 gm, 2 m), (3) TBI plus 30 min of hypoxia (PaO2, ~40 mm Hg) and hypotension (mean arterial blood pressure, ~40 mm Hg) (THH), and (4) HH alone. The baseline value for dialysate NAA (NAA(d)) in the rats was 8.17 ± μM. No significant difference between groups was found for this baseline value. The TBI group had a modest (100%) transient increase in NAA(d) after isolated TBI. The HH group had a transient (500%) increase in NAA(d) at 1 h, sustained for 2 h. In the THH group, there was a persistent increase in NAA(d) (800%) that peaked at 2.5 h. The whole brain NAA (NAA(w)) concentration in controls was 8.5 ± 0.5 mmol/kg wet weight. There was no significant difference between TBI and controls; however, there was a significant decrease in NAA(w) in the THH and HH group compared to controls. Thus, in this animal model of TBI and TBI with secondary insult, we found that persistent, marked elevation in NAA is associated with TBI and secondary ischemic/hypoxic insult, but not with isolated TBI alone.

Original languageEnglish
Pages (from-to)31-39
Number of pages9
JournalJournal of Neurotrauma
Volume17
Issue number1
StatePublished - Jan 1 2000
Externally publishedYes

Fingerprint

Brain Injuries
Biomarkers
Hypotension
N-acetylaspartate
Traumatic Brain Injury
Arterial Pressure
Animal Models
Dialysis Solutions
Brain
High Pressure Liquid Chromatography
Hypoxia
Weights and Measures

Keywords

  • High-performance liquid chromatography
  • Microdialysis
  • N-acetyl-aspartate
  • Traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury. / Al-Samsam, Rim H.; Alessandri, Beat; Bullock, Ross.

In: Journal of Neurotrauma, Vol. 17, No. 1, 01.01.2000, p. 31-39.

Research output: Contribution to journalArticle

@article{699e99e084ff4c9e98a450a705c51aba,
title = "Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury",
abstract = "We evaluated the acute changes in interstitial and whole brain N-acetyl- aspartate (NAA) measured by high-performance liquid chromatography in animal models of isolated traumatic brain injury (TBI) and TBI combined with secondary insult (hypotension-hypoxia [HH]). The Marmarou impact-acceleration model was used. Four groups were studied: (1) sham-operated control, (2) TBI alone (TBI 500 gm, 2 m), (3) TBI plus 30 min of hypoxia (PaO2, ~40 mm Hg) and hypotension (mean arterial blood pressure, ~40 mm Hg) (THH), and (4) HH alone. The baseline value for dialysate NAA (NAA(d)) in the rats was 8.17 ± μM. No significant difference between groups was found for this baseline value. The TBI group had a modest (100{\%}) transient increase in NAA(d) after isolated TBI. The HH group had a transient (500{\%}) increase in NAA(d) at 1 h, sustained for 2 h. In the THH group, there was a persistent increase in NAA(d) (800{\%}) that peaked at 2.5 h. The whole brain NAA (NAA(w)) concentration in controls was 8.5 ± 0.5 mmol/kg wet weight. There was no significant difference between TBI and controls; however, there was a significant decrease in NAA(w) in the THH and HH group compared to controls. Thus, in this animal model of TBI and TBI with secondary insult, we found that persistent, marked elevation in NAA is associated with TBI and secondary ischemic/hypoxic insult, but not with isolated TBI alone.",
keywords = "High-performance liquid chromatography, Microdialysis, N-acetyl-aspartate, Traumatic brain injury",
author = "Al-Samsam, {Rim H.} and Beat Alessandri and Ross Bullock",
year = "2000",
month = "1",
day = "1",
language = "English",
volume = "17",
pages = "31--39",
journal = "Journal of Neurotrauma",
issn = "0897-7151",
publisher = "Mary Ann Liebert Inc.",
number = "1",

}

TY - JOUR

T1 - Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury

AU - Al-Samsam, Rim H.

AU - Alessandri, Beat

AU - Bullock, Ross

PY - 2000/1/1

Y1 - 2000/1/1

N2 - We evaluated the acute changes in interstitial and whole brain N-acetyl- aspartate (NAA) measured by high-performance liquid chromatography in animal models of isolated traumatic brain injury (TBI) and TBI combined with secondary insult (hypotension-hypoxia [HH]). The Marmarou impact-acceleration model was used. Four groups were studied: (1) sham-operated control, (2) TBI alone (TBI 500 gm, 2 m), (3) TBI plus 30 min of hypoxia (PaO2, ~40 mm Hg) and hypotension (mean arterial blood pressure, ~40 mm Hg) (THH), and (4) HH alone. The baseline value for dialysate NAA (NAA(d)) in the rats was 8.17 ± μM. No significant difference between groups was found for this baseline value. The TBI group had a modest (100%) transient increase in NAA(d) after isolated TBI. The HH group had a transient (500%) increase in NAA(d) at 1 h, sustained for 2 h. In the THH group, there was a persistent increase in NAA(d) (800%) that peaked at 2.5 h. The whole brain NAA (NAA(w)) concentration in controls was 8.5 ± 0.5 mmol/kg wet weight. There was no significant difference between TBI and controls; however, there was a significant decrease in NAA(w) in the THH and HH group compared to controls. Thus, in this animal model of TBI and TBI with secondary insult, we found that persistent, marked elevation in NAA is associated with TBI and secondary ischemic/hypoxic insult, but not with isolated TBI alone.

AB - We evaluated the acute changes in interstitial and whole brain N-acetyl- aspartate (NAA) measured by high-performance liquid chromatography in animal models of isolated traumatic brain injury (TBI) and TBI combined with secondary insult (hypotension-hypoxia [HH]). The Marmarou impact-acceleration model was used. Four groups were studied: (1) sham-operated control, (2) TBI alone (TBI 500 gm, 2 m), (3) TBI plus 30 min of hypoxia (PaO2, ~40 mm Hg) and hypotension (mean arterial blood pressure, ~40 mm Hg) (THH), and (4) HH alone. The baseline value for dialysate NAA (NAA(d)) in the rats was 8.17 ± μM. No significant difference between groups was found for this baseline value. The TBI group had a modest (100%) transient increase in NAA(d) after isolated TBI. The HH group had a transient (500%) increase in NAA(d) at 1 h, sustained for 2 h. In the THH group, there was a persistent increase in NAA(d) (800%) that peaked at 2.5 h. The whole brain NAA (NAA(w)) concentration in controls was 8.5 ± 0.5 mmol/kg wet weight. There was no significant difference between TBI and controls; however, there was a significant decrease in NAA(w) in the THH and HH group compared to controls. Thus, in this animal model of TBI and TBI with secondary insult, we found that persistent, marked elevation in NAA is associated with TBI and secondary ischemic/hypoxic insult, but not with isolated TBI alone.

KW - High-performance liquid chromatography

KW - Microdialysis

KW - N-acetyl-aspartate

KW - Traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=0033963852&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033963852&partnerID=8YFLogxK

M3 - Article

VL - 17

SP - 31

EP - 39

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 1

ER -