Abstract 14316: Effect of Residual Cerebral Blood Flow During Ischemic Depolarization on Neuronal Cell Damage in Rats
Introduction: High-quality chest compression can maintain the membrane potential in neuronal cells. However, it is unknown whether low-quality chest compression that cannot maintain the membrane potential is worth performing for brain protection. Low residual cerebral blood flow (CBF) could be harmful because of excess supply of glucose and calcium. In the present study, we observed the effects of low CBF on extracellular glutamate concentrations and the degree of neuronal cell damage by comparing two groups that had different residual CBF.
Methods: Extracellular potential (DC-potential), CBF, and extracellular glutamate concentration were measured at the same site in the parietal cerebral cortex. CBF was reduced by bilateral occlusion of the common carotid arteries and exsanguination until the DC-potential showed a loss of membrane potential (low-flow group, n = 9), or CBF was further reduced by 5-10% of pre-ischemia (severe-low-flow group, n = 9). After 10 minutes of ischemic insult, CBF was restored promptly. Histological outcome was evaluated 5 days later.
Results: The threshold for a loss of membrane potential was 27 ± 14% of the pre-ischemia level. The mean CBF during ischemic insult was 20 ± 5% of the pre-ischemia level in the low-flow group, and 13 ± 4% in the severe-low-flow group (p = 0.0002). The maximum extracellular glutamate concentration was significantly higher in the severe-low-flow group (326 ± 117 μmol/L) compared to the low-flow group (78 ± 62 μmol/L, p < 0.00001). Neuronal cells were significantly more damaged in the severe-low-flow group (44 ± 9%) compared to the low-flow group (15 ± 5%, p < 0.00001). There were significant correlations between residual CBF and extracellular glutamate concentration (r2 = 0.68, p < 0.0001), and between the degree of neuronal cell damage and the maximum extracellular glutamate concentration (r2 = 0.58, p < 0.001).
Conclusions: The present study indicates that low residual CBF is used for glutamate uptake, and contributes to neuroprotection. Therefore, even low-quality chest compression could be worth performing for neuroprotection.
Author Disclosures: H. Kawase: None. Y. Takeda: None. R. Mizoue: None. S. Sato: None. M. Fushimi: None. H. Morimatsu: None.
- © 2016 by American Heart Association, Inc.