EFFECTS OF HYPOTHERMIC METABOLIC SUPPRESSION ON HIPPOCAMPAL GLUTAMATECONCENTRATIONS AFTER TRANSIENT GLOBAL CEREBRAL-ISCHEMIA

The cerebroprotective effects of mild and moderate hypothermia cannot be explained solely by a temperature-induced decrease in cerebral meta bolic rate. This study examined the effects of graded hypothermia (32 degrees C, 28 degrees C, and 22 degrees C, vs 38 degrees C) on periisc hemic extracellular hippocampal glutamate concentrations in the New Ze aland White rabbit. Global cerebral ischemia (15 min) was produced by a combination of neck tourniquet inflation and induction of systemic h ypotension. Glutamate, an important mediator of ischemic neuronal inju ry, was measured using in vivo microdialysis and high-performance liqu id chromatography. Mean extracellular glutamate concentrations increas ed by 11 mu M in the 38 degrees C group during the ischemic period. Gl utamate increased by <1 mu M in the 32 degrees C and 28 degrees C grou ps and by 3 mu M in the 22 degrees C group. Thus, mild degrees of hypo thermia profoundly reduced glutamate release during ischemia. This red uction greatly exceeded the estimated temperature-induced decrease in cerebral metabolic rate. We conclude that hypothermic inhibition of gl utamate release during episodes of transient ischemia may significantl y contribute to neuronal protection.