title: Dexmedetomidine weakens dynamic cerebral autoregulation as assessed by transfer function analysis and the thigh cuff method.
abstract: BACKGROUND
  Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation.
  
  
  METHODS
  Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.2 microg x kg(-1) x h(-1) for 60 min), and high-dose dexmedetomidine (loading, 6 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.4 microg x kg(-1) x h(-1) for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method.
  
  
  RESULTS
  Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release.
  
  
  CONCLUSIONS
  Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.
authors.affiliation: Department of Social Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: Yojiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Iwasaki
authors.forename: Ken
authors.initials: K
authors.lastname: Aoki
authors.forename: Wakako
authors.initials: W
authors.lastname: Kojima
authors.forename: Jitsu
authors.initials: J
authors.lastname: Kato
authors.forename: Setsuro
authors.initials: S
authors.lastname: Ogawa
mesh_terms: D000293:Adolescent; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D018592:Cross-Over Studies; D020927:Dexmedetomidine / Q000494:pharmacology*; D004311:Double-Blind Method; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D008297:Male; D012119:Respiration / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000316:Adrenergic alpha-Agonists; D020927:Dexmedetomidine