Hypothermia prevents ischemia-induced increases in hippocampal glycine concentrations in rabbits.
Author(s) -
Andrew Baker,
Mark H. Zornow,
Marjorie R. Grafe,
M S Scheller,
Stephen R. Skilling,
David H. Smullin,
Alice A. Larson
Publication year - 1991
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.22.5.666
Subject(s) - microdialysis , hypothermia , medicine , neuroprotection , glutamate receptor , glycine , ischemia , anesthesia , nmda receptor , hippocampal formation , in vivo , extracellular , pharmacology , amino acid , endocrinology , biochemistry , central nervous system , receptor , biology , microbiology and biotechnology
We subjected 10 New Zealand White rabbits to 10 minutes of global cerebral ischemia under either normothermic (37 degrees C) or moderately hypothermic (29 degrees C) conditions. Hippocampal concentrations of glutamate, aspartate, and glycine were monitored using in vivo microdialysis. Outcome was assessed by both neurological and neuropathologic criteria. Hypothermia afforded nearly complete protection from ischemic injury. Ischemia-induced increases in the concentrations of glutamate, aspartate, and glycine in the normothermic group (3, 12, and 3 times baseline) were strikingly attenuated in the hypothermic group. In addition, the prolonged postischemic elevation of glycine levels seen in the normothermic group was absent in the hypothermic group. These results suggest that the neuroprotective properties of hypothermia may reside, in part, in their ability to prevent increases in the extracellular concentrations of amino acids that enhance the activity of the N-methyl-D-aspartate receptor complex.
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