title: Cerebral Blood Flow Threshold Is Higher for Membrane Repolarization Than for Depolarization and Is Lowered by Intraischemic Hypothermia in Rats.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  Prospective animal study.
  
  
  METHODS
  Experimental laboratory in a university hospital.
  
  
  METHODS
  Male Sprague-Dawley rats (n = 40).
  
  
  METHODS
  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).
  
  
  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.
authors.affiliation: 1Department of Anesthesiology, Okayama University Medical School, Okayama City, Okayama, Japan. 2Department of Anesthesiology and Intensive Care Medicine, Kawasaki Medical School, Kurashiki, Okayama, Japan.
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Mizoue
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Takeda
authors.forename: Sachiko
authors.initials: S
authors.lastname: Sato
authors.forename: Ken
authors.initials: K
authors.lastname: Takata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morimatsu
mesh_terms: D000818:Animals; D001921:Brain / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology / Q000628:therapy*; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D007036:Hypothermia, Induced / Q000379:methods*; D017078:Laser-Doppler Flowmetry; D008297:Male; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors