title: Effect of dexmedetomidine on cerebral blood flow velocity, cerebral metabolic rate, and carbon dioxide response in normal humans.
abstract: BACKGROUND
  Dexmedetomidine reduces cerebral blood flow (CBF) in humans and animals. In animal investigations, cerebral metabolic rate (CMR) was unchanged. Therefore, the authors hypothesized that dexmedetomidine would cause a decrease in the CBF/CMR ratio with even further reduction by superimposed hyperventilation. This reduction might be deleterious in patients with neurologic injuries.
  
  
  METHODS
  Middle cerebral artery velocity (CBFV) was recorded continuously in six volunteers. CBFV, jugular bulb venous saturation (Sjvo2), CMR equivalent (CMRe), and CBFV/CMRe ratio were determined at six intervals before, during, and after administration of dexmedetomidine: (1) presedation; (2) presedation with hyperventilation; at steady state plasma levels of (3) 0.6 ng/ml and (4) 1.2 ng/ml; (5) 1.2 ng/ml with hyperventilation; and (6) 30 min after discontinuing dexmedetomidine. The slope of the arterial carbon dioxide tension (Paco2)-CBFV relation was determined presedation and at 1.2 ng/ml.
  
  
  RESULTS
  CBFV and CMRe decreased in a dose-related manner. The CBFV/CMRe ratio was unchanged. The CBFV response to carbon dioxide decreased from 1.20 +/- 0.2 cm.s.mm Hg presedation to 0.40 +/- 0.15 cm.s.mm Hg at 1.2 ng/ml. Sjvo2 was statistically unchanged during hyperventilation at 1.2 ng/ml versus presedation (50 +/- 11 vs. 43 +/- 5%). Arousal for hyperventilation at 1.2 ng/ml resulted in increased CBFV (30 +/- 5 to 38 +/- 4) and Bispectral Index (43 +/- 10 to 94 +/- 3).
  
  
  CONCLUSIONS
  The predicted decrease in CBFV/CMRe ratio was not observed because of an unanticipated reduction of CMRe and a decrease in the slope of the Paco2-CBFV relation. CBFV and Bispectral Index increases during arousal for hyperventilation at 1.2 ng/ml suggest that CMR-CBF coupling is preserved during dexmedetomidine administration. Further evaluation of dexmedetomidine in patients with neurologic injuries seems justified.
authors.affiliation: Veterans Affairs Medical Center, San Diego, California 92161, USA. jdrummond@ucsd.edu
authors.forename: John C
authors.initials: JC
authors.lastname: Drummond
authors.forename: Andrew V
authors.initials: AV
authors.lastname: Dao
authors.forename: David M
authors.initials: DM
authors.lastname: Roth
authors.forename: Ching-Rong
authors.initials: CR
authors.lastname: Cheng
authors.forename: Benjamin I
authors.initials: BI
authors.lastname: Atwater
authors.forename: Anushirvan
authors.initials: A
authors.lastname: Minokadeh
authors.forename: Leonardo C
authors.initials: LC
authors.lastname: Pasco
authors.forename: Piyush M
authors.initials: PM
authors.lastname: Patel
mesh_terms: D000328:Adult; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology*; D001783:Blood Flow Velocity / Q000187:drug effects*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002245:Carbon Dioxide / Q000378:metabolism*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D020927:Dexmedetomidine / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D013055:Spectrophotometry, Infrared
chemical_list: D018712:Analgesics, Non-Narcotic; D002245:Carbon Dioxide; D020927:Dexmedetomidine