Abstract: We have used microdialysis to establish an experimental model to characterize mechanisms whereby released substances cause secondary damage in spinal cord injury. We use this model here to characterize damaging effects of the hydroxyl radical (OH') in vivo in the spinal cord. OH'was generatad in vivo by pumping H2O2 and FeCI2/EDTA through parallel microdialysis fibers inserted into the spinal cord. These agents mixed in the tissue to produce OH'by Fenton's reaction. Two types of control experiments were also conducted, one administering only 5 mM H2O2 and the other only 0.5 mM FeCI2/0.82 mM EDTA. During administration of these chemicals, electrical conduction was recorded as one test for deterioration. OH'blocked conduction completely in 2.5‐5 h and Fe2+/EDTA partly blocked conduction, but H2O2 alone did not cause detectable blockage. Histological examination supported the hypothesis that neurons were killed by OH', as Fe2+/EDTA and H2O2 alone did not destroy significant numbers of neurons. OH', H2O2, and Fe2+ all caused gradual increases in extracellular amino acid levels. These results are consistent with Fe2+‐catalyzed free radical generation playing a role in tissue damage upon spinal cord injury.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of neurochemistry|
|State||Published - Jan 1994|
- Amino acid release
- Evoked potential
- Hydroxyl radical
- Neuron death.
- Secondary spinal cord injury
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience