INTRAISCHEMIC HYPOTHERMIA DECREASES THE RELEASE OF GLUTAMATE IN THE CORES OF PERMANENT FOCAL CEREBRAL INFARCTS

Citation
Cj. Baker et al., INTRAISCHEMIC HYPOTHERMIA DECREASES THE RELEASE OF GLUTAMATE IN THE CORES OF PERMANENT FOCAL CEREBRAL INFARCTS, Neurosurgery, 36(5), 1995, pp. 994-1001
Citations number
66
Categorie Soggetti
Surgery,Neurosciences
Journal title
ISSN journal
0148396X
Volume
36
Issue
5
Year of publication
1995
Pages
994 - 1001
Database
ISI
SICI code
0148-396X(1995)36:5<994:IHDTRO>2.0.ZU;2-T
Abstract
THE CEREBROPROTECTIVE EFFECTS of hypothermia in focal models of ischem ia are well established, but little is known about the underlying mech anisms of this form of brain protection. Cortical cooling in global tr ansient ischemic models suggests that hypothermia limits glutamate exc itotoxicity by decreasing the release of glutamate during ischemia. Fe w studies have examined glutamate release in the more physiological mo del of permanent focal ischemia. In this study, we used a rat model of middle cerebral artery occlusion (MCAO) of permanent focal ischemia. Extracellular glutamate concentration was analyzed bilaterally by micr odialysis for 30 minutes before MCAO to 120 minutes after MCAO. Normot hermic animals (n = 13) had a baseline glutamate concentration of 9.23 +/- 2.5 mu mol/ml (mean +/- standard error of the mean) before MCAO. Extracellular glutamate rose quickly after vessel occlusion and peaked at 33.95 +/- 6.3 mu mol/ml 30 minutes after MCAO. By 60 minutes after MCAO, this level had decreased to 25.14 +/- 6.3 mu mol/ml; glutamate levels decreased slightly to 21.35 +/- 6.8 mu mol/ml by 120 minutes. H ypothermic animals (n = 11) had an initial extracellular glutamate con centration of 5.22 +/- 1.3 mu mol/ml before MCAO. This value rose grad ually to a maximum of 10.69 +/- 3.3 mu m/ml at 50 minutes after MCAO a nd then returned to a baseline value of 2.58 +/- 1.2 mu mol/ml by 120 minutes. Contralateral control glutamate dialysates in the normothermi c and hypothermic groups remained near baseline throughout the experim ental period. The mean percentages of right hemispheric volumes occupi ed by infarcts were 11.96 +/- 1.68% in the hypothermic group and 19.77 +/- 2.03% in the normothermic animals. Hypothermia seems to decrease the peak and duration of extracellular glutamate efflux in the core of permanent focal infarcts. This decrease in the diffusable pool of cor e glutamate may have implications for penumbral tissue viability.