1994 Volume 1 Issue 1 Pages 21-25
Neurologic deficits are a major source of serious morbidity in patients resuscitated from cardiac arrest. Recent evidences support the hypothesis that accumulation of excitatory amino acids and overstimulation of their receptors in the brain tissue contribute to ischemic neuronal damage. In the present study, we measured concentrations of amino acid neurotransmitters, including glutamate and aspartate, in human cerebrospinal fluid (CSF) following cardiopulmonary resuscitation (CPR) to clarify whether CSF levels of excitatory amino acids reflect the global ischemic insults during cardiac arrest. In 11 post-CPR patients without any evidence of intracranial causes of cardiac arrest (the CPR group), CSF was sampled 2 to 12 hours following CPR. After deproteinization and storage at-80°C, derivatization, elution, and analysis of amino acids in CSF samples were performed by high-performance liquid chromatography. Sixteen patients scheduled for spinal anesthesia and elective surgery were regarded as normal control (the control group).
The results showed that glutamate and aspartate in the CSF of the CPR group significantly increased 3.6 and 5.7-fold com pared with fhose the control group. Taurine and alanine also significantly increased. Thus, in the present clinical study, we demonstrated elevations of neurotoxic glutamate and aspartate in CSF following CPR, which might relate post-CPR neurologic deficits.