• Ryoichi Mizoue, Yoshimasa Takeda, Sachiko Sato, Ken Takata, and Hiroshi Morimatsu.
• 1Department of Anesthesiology, Okayama University Medical School, Okayama City, Okayama, Japan. 2Department of Anesthesiology and Intensive Care Medicine, Kawasaki Medical School, Kurashiki, Okayama, Japan.
• Crit. Care Med. 2015 Sep 1;43(9):e350-5.

ObjectivesTo evaluate the cerebral blood flow thresholds for membrane depolarization and repolarization and the effect of brain hypothermia on the cerebral blood flow threshold for membrane repolarization.DesignProspective animal study.SettingExperimental laboratory in a university hospital.SubjectsMale Sprague-Dawley rats (n = 40).InterventionsCerebral blood flow and membrane depolarization and repolarization in the cerebral cortex were simultaneously monitored by laser Doppler and extracellular potential, respectively. Following bilateral occlusion of the common carotid arteries, cerebral blood flow was decreased by draining blood at a rate of 2.5% of the control level/min until membrane depolarization was initiated. At 5 and 10 minutes (Normothermia 5 and Normothermia 10 groups, respectively) after depolarization onset, cerebral blood flow was restored at the same rate until membrane repolarization was observed. In some animals, intraischemic brain hypothermia targeting 31°C was initiated immediately after the onset of depolarization (Hypothermia 5 and Hypothermia 10 groups).Measurements And Main ResultsThe cerebral blood flow threshold for repolarization (46.5% ± 12%) was significantly higher than that for depolarization (18.9% ± 4.8%; p < 0.01) in the Normothermia 5 group and was further increased to 61.5% ± 14% (p < 0.01) in the Normothermia 10 group. With initiation of hypothermia, the cerebral blood flow threshold for membrane repolarization was suppressed to 33.8% ± 10% in the Hypothermia 5 group (p < 0.01 vs Normothermia 5 group) and was unaltered by prolongation of ischemia (Hypothermia 10 group; 36.6% ± 6%).ConclusionsCerebral blood flow thresholds were significantly higher for repolarization than for depolarization and were further increased by prolonged ischemia. Intraischemic brain hypothermia decreased the repolarization threshold and abrogated the increase in the repolarization threshold caused by prolonged ischemia.

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