Fluorometric assay of nitrite and nitrate in brain tissue after traumatic brain injury and cerebral ischemia

Fluorometric assay of nitrite and nitrate in brain tissue after traumatic brain injury and... Nitric oxide synthase (NOS) is distributed within the brain, and nitric oxide (NO) is felt to be involved in the pathophysiology of deterioration after head injury and cerebral ischemia. This study determined the levels of the stable end products of NOS (NO x =nitrite+nitrate) after traumatic brain injury (TBI) and transient cerebral ischemia. A fluorometric assay using nitrate reductase and the NADPH regenerating system was used to quantitate NO x in ultrafiltered (10-kDa cutoff) cortical and hippocampal extracts after reduction of nitrate. In TBI rats, both the plasma and tissue showed a sharp increase in NO x levels 5 min after injury. Plasma NO x returned to control levels by 2 h after injury. Ipsilateral-cortex NO x levels returned to control levels ∼6 h after injury and remained constant from 6–24 h. Contralateral-cortex returned near to control levels after 1 h. Hippocampus also followed a similar trend. In gerbils, there was a significant elevation in tissue NO x levels immediately after 10 min transient cerebral ischemia, which gradually returned to control levels over 24 h reperfusion. This striking burst of NO synthesis immediately after injury is clearly evident whether the injury is head trauma or ischemia, or whether the measurements were performed on tissue or plasma. It is unknown whether endothelial NOS, neuronal NOS, or both caused the elevation of the NO end products seen after the CNS insults. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Fluorometric assay of nitrite and nitrate in brain tissue after traumatic brain injury and cerebral ischemia

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Publisher
Elsevier
Copyright
Copyright © 1998 Elsevier Science B.V.
ISSN
0006-8993
D.O.I.
10.1016/S0006-8993(98)00183-8
Publisher site
See Article on Publisher Site

Abstract

Nitric oxide synthase (NOS) is distributed within the brain, and nitric oxide (NO) is felt to be involved in the pathophysiology of deterioration after head injury and cerebral ischemia. This study determined the levels of the stable end products of NOS (NO x =nitrite+nitrate) after traumatic brain injury (TBI) and transient cerebral ischemia. A fluorometric assay using nitrate reductase and the NADPH regenerating system was used to quantitate NO x in ultrafiltered (10-kDa cutoff) cortical and hippocampal extracts after reduction of nitrate. In TBI rats, both the plasma and tissue showed a sharp increase in NO x levels 5 min after injury. Plasma NO x returned to control levels by 2 h after injury. Ipsilateral-cortex NO x levels returned to control levels ∼6 h after injury and remained constant from 6–24 h. Contralateral-cortex returned near to control levels after 1 h. Hippocampus also followed a similar trend. In gerbils, there was a significant elevation in tissue NO x levels immediately after 10 min transient cerebral ischemia, which gradually returned to control levels over 24 h reperfusion. This striking burst of NO synthesis immediately after injury is clearly evident whether the injury is head trauma or ischemia, or whether the measurements were performed on tissue or plasma. It is unknown whether endothelial NOS, neuronal NOS, or both caused the elevation of the NO end products seen after the CNS insults.

Journal

Brain ResearchElsevier

Published: May 18, 1998

References

  • The biphasic opening of the blood–brain barrier in the cortex and hippocampus after traumatic brain injury in rats
    Baskaya, M.K.; Rao, A.M.; Dogan, A.; Donaldson, D.; Dempsey, R.J.
  • Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis
    Benveniste, H.; Drejer, J.; Schouboe, A.; Diemer, N.H.
  • Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage
    Dhillion, H.S.; Dose, J.M.; Scheff, S.W.; Prasad, M.R.
  • Generation of nitric oxide and superoxide during reperfusion after focal cerebral ischemia in rats
    Kumura, E.; Yoshimine, T.; Iwatsuki, K-I.; Yamanaka, K.; Tanaka, S.; Hayakawa, T.; Shiga, T.; Kosaka, H.
  • Induction of nitric oxide synthase activity in rodent brain following cerebral artery occlusion
    Yoshida, T.; Waeber, C.; Huang, Z.; Moskowitz, M.A.

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