Abstract |
1. Spinal cord ischemia evoked a biphasic increase in CSF-Glu during 20 min of ischemia (40%) and at 2 hr after reperfusion (70%) in the nontreated group that was attenuated by all treated groups. But MK-801 (15 micrograms i.t.) did not affect the increased Glu at 2 hr (80%). 2. The argyrophilia observed in laminae II-V at 8 hr after reperfusion was attenuated by hypothermia (33 degrees C) and combination with MK-801, but the attenuation was less with MK-801. 3. Mild hypothermia attenuated the biphasic increase in CSF-Glu and corresponding development of neuronal damage after spinal cord ischemia. 4. Mild hypothermia with NMDA antagonism did not yield any further effects, suggesting that hypothermia itself plays a pivotal role in the protection.
|
Authors | T Ishikawa, M Marsala |
Journal | Cellular and molecular neurobiology
(Cell Mol Neurobiol)
Vol. 19
Issue 2
Pg. 199-208
(Apr 1999)
ISSN: 0272-4340 [Print] United States |
PMID | 10081604
(Publication Type: Journal Article)
|
Chemical References |
- Excitatory Amino Acid Antagonists
- Receptors, N-Methyl-D-Aspartate
- Glutamic Acid
- Dizocilpine Maleate
|
Topics |
- Animals
- Combined Modality Therapy
- Denervation
- Dizocilpine Maleate
(pharmacology)
- Excitatory Amino Acid Antagonists
(pharmacology)
- Glutamic Acid
(cerebrospinal fluid, metabolism)
- Hypothermia, Induced
- Injections, Spinal
- Male
- Microdialysis
- Nerve Degeneration
(drug therapy, physiopathology, prevention & control)
- Rats
- Rats, Sprague-Dawley
- Receptors, N-Methyl-D-Aspartate
(physiology)
- Reperfusion Injury
(drug therapy, physiopathology)
- Spinal Cord
(blood supply, chemistry, physiopathology)
|