Abstract

Introduction: It has been reported that cerebral blood flow (CBF) supplied by chest compression (20-40% of control levels) exceeds the CBF threshold for membrane depolarization (20%). However, the CBF threshold for membrane repolarization has not been studied. It is unknown whether chest compression can restore membrane potential. In the present study, we compared the CBF threshold for depolarization with that for repolarization. In addition, the effects of brain hypothermia on the repolarization threshold were evaluated. Methods: Rats (10 in each group) were anesthetized with isoflurane. CBF was measured by placing a laser-Doppler flow probe placed adjacent to a direct current (DC) potential electrode in the parietal cerebral cortex. Following bilateral occlusion of common carotid artery, CBF was continuously decreased by exsanguination at a speed of 5% of the baseline level every 2 min until a sudden negative DC shift was observed. After 5 or 10 min of ischemic depolarization, the CBF was restored at the same rate by returning blood until a positive DC shift was observed. In the hypothermia groups, brain temperature was decreased to 31°C by initiating nasopharyngeal cooling after depolarization. Result: The threshold for repolarization (46.5 ± 12%) was significantly higher than that for depolarization (19.2 ± 5%, p < 0.001) after 5 min of depolarization time, and further increased to 61.5 ± 14% (p < 0.05) after 10 min of depolarization time. Brain hypothermia significantly decreased the threshold for repolarization (5 min of ischemic depolarization: 33.8 ± 10%, p < 0.05 compared with normal temperature, 10 min: 36.6 ± 6%, p < 0.05). Conclusion: Thresholds for repolarization were significantly higher than those for depolarization and are likely to exceed the levels supplied by chest compression. Induced brain hypothermia during ischemia lowered CBF thresholds for repolarization and may help protect the brain during CPR.

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