Cardiopulmonary Resuscitation May Not Stop Glutamate Release in the Cerebral Cortex

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.