(Stroke. 1996;27:913-918.)
© 1996 American Heart Association, Inc.
Articles |
Effects of Hypothermia on the Rate of Excitatory Amino Acid Release After Ischemic Depolarization
From the Neuroanesthesia Research Laboratory, Department of Anesthesia, University of Iowa College of Medicine (Iowa City). K.N. was a research fellow from the Critical Care Medical Center, Yamaguchi University, Ube, Yamaguchi, Japan.
Correspondence to Michael Todd, MD, Department of Anesthesia, 6JCP, University of Iowa Hospitals and Clinics, Iowa City, IA 52242. E-mail mtodd@blue.weeg.uiowa.edu.
Background and Purpose Hypothermia slows the increase in extracellular excitatory amino acid (EAA) concentrations during temporary cerebral ischemia. However, it is unclear whether hypothermia slows the rate of EAA release or just delays the time until the first sharp increase (which occurs coincident with terminal depolarization).
Methods Pericranial temperatures were adjusted to 38°C,
34°C, 31°C, or 25°C in halothane-anesthetized rats.
The cortical DC voltage was recorded from a glass microelectrode
while the cortical concentrations of glutamate, aspartate, glycine, and
-aminobutyric acid (GABA) were measured by microdialysis. A
cardiac arrest was induced with intravenous KCl, and the
times until electroencephalograph isoelectricity and terminal
depolarization were recorded. Dialysate concentrations of the four
compounds were measured at 10, 20, and 30 minutes after depolarization.
Results The times to isoelectricity and depolarization varied inversely with temperature; depolarization time increased from 70±9 seconds at 38°C (mean±SD) to 294±34 seconds at 25°C. The dialysate concentrations of all four compounds increased during ischemia, and the rate of increase was inhibited by cooling. After 30 minutes of ischemia, glutamate concentration in 38°C animals was 58.4±31.8 µmol/L; this decreased to 15.9±8.4 µmol/L at 25°C. The magnitude of the effects of temperature on amino acid release differed with the compound measured. For glutamate, the calculated Q10 was 3.63. Corresponding values for aspartate and glycine were 3.68 and 1.95, respectively. By contrast, Q10 for GABA release was 6.31, indicating greater sensitivity to cooling.
Conclusions These results suggest that effects of hypothermia on EAA concentrations during cerebral ischemia may be the result of both a delay until initial EAA release as well as a direct effect of temperature on the rate of amino acid release. The observed temperature effects are more consistent with carrier-mediated processes controlling EAA release.
Key Words: cerebral ischemia, global • excitatory amino acids • glutamates • hypothermia • rats
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