Cerebral Blood Flow Threshold Is Higher for Membrane Repolarization Than for Depolarization and Is Lowered by Intraischemic Hypothermia in Rats.

OBJECTIVES To 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. DESIGN Prospective animal study. SETTING Experimental laboratory in a university hospital. SUBJECTS Male Sprague-Dawley rats (n = 40). INTERVENTIONS Cerebral 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 RESULTS The 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%). CONCLUSIONS Cerebral 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.