Cardiopulmonary Resuscitation May Not Stop Glutamate Release in the Cerebral Cortex.

Abstract

Cardiopulmonary 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. Extracellular 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. Glutamate 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. CPR alone reduced the progression of brain damage for a limited period but CPR in combination with brain cooling strongly suppressed increases in glutamate levels.