Abstract 13443: Intraischemic Nasopharyngeal Cooling Decreases Extracellular Glutamate Level and the Cerebral Blood Flow Threshold for Repolarization
Introduction: Induction of intraischemic hypothermia is an effective therapy for neuroprotection. We found that brain hypothermia induced after depolarization lowers the cerebral blood flow (CBF) threshold for repolarization. In this study, we examined the effect of nasopharyngeal cooling on extracellular glutamate level at repolarization onset.
Methods: Rats were divided into the normothermic (control) and hypothermic groups (7 rats in each). A microdialysis probe for measuring glutamate levels was inserted in the right parietal cortex adjacent to the direct current (DC) electrode and laser- Doppler flow probe. Following bilateral common carotid artery occlusion, the CBF was continuously decreased by exsanguination at a speed of 5% of the baseline level every 2 min until depolarization occurred. After 5 min of ischemic depolarization, the CBF was restored at the same rate until a positive DC shift was observed. In the hypothermic group, the brain temperature was decreased to 31°C by initiating nasopharyngeal cooling immediately after depolarization onset.
Results: In the hypothermic group, the brain temperature reduced to 31°C at 4.7 ± 0.5 min after the onset of nasopharyngeal cooling. The maximum extracellular glutamate level was significantly lower for the hypothermic group (169.6 ± 120.7 μmol/L) than for control (357.7 ± 104.7 μmol/L, p < 0.01). The time to reach this level was lesser for the hypothermic group (7.8 ± 2.5 min) than for control (9.9 ± 2.9 min), but the intergroup difference was not significant. The extracellular glutamate level at the start of repolarization and the CBF threshold was lower for the hypothermic group than the normothermic group (147.0 ± 108.1 μmol/L vs. 303.2 ± 91.3 μmol/L, p = 0.01; 24.0 ± 7% vs. 43.1 ± 20%, p = 0.03).
Conclusion: Decreased extracellular glutamate levels after intraischemic nasopharyngeal cooling may be involved in the mechanisms underlying the decrease in the CBF threshold for repolarization.
- © 2013 by American Heart Association, Inc.