• Miki Fushimi, Yoshimasa Takeda, Ryoichi Mizoue, Sachiko Sato, Hirokazu Kawase, Yuji Takasugi, Satoshi Murai, and Hiroshi Morimatsu.
• Departments of Anesthesiology and Resuscitology.
• J Neurosurg Anesthesiol. 2023 Jul 1; 35 (3): 341346341-346.

BackgroundCardiopulmonary resuscitation (CPR) may not be sufficient to halt the progression of brain damage. Using extracellular glutamate concentration as a marker for neuronal damage, we quantitatively evaluated the degree of brain damage during resuscitation without return of spontaneous circulation.Materials And MethodsExtracellular cerebral glutamate concentration was measured with a microdialysis probe every 2 minutes for 40 minutes after electrical stimulation-induced cardiac arrest without return of spontaneous circulation in Sprague-Dawley rats. The rats were divided into 3 groups (7 per group) according to the treatment received during the 40 minutes observation period: mechanical ventilation without chest compression (group V); mechanical ventilation and chest compression (group VC) and; ventilation, chest compression and brain hypothermia (group VCH). Chest compression (20 min) and hypothermia (40 min) were initiated 6 minutes after the onset of cardiac arrest.ResultsGlutamate concentration increased in all groups after cardiac arrest. Although after the onset of chest compression, glutamate concentration showed a significant difference at 2 min and reached the maximum at 6 min (VC group; 284±48 μmol/L vs. V group 398±126 μmol/L, P =0.003), there was no difference toward the end of chest compression (513±61 μmol/L vs. 588±103 μmol/L, P =0.051). In the VCH group, the initial increase in glutamate concentration was suddenly suppressed 2 minutes after the onset of brain hypothermia.ConclusionsCPR alone reduced the progression of brain damage for a limited period but CPR in combination with brain cooling strongly suppressed increases in glutamate levels.Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.

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