title: Low-dose dexmedetomidine facilitates the carotid body response to low oxygen tension in vitro via α2-adrenergic receptor activation in rabbits.
abstract: BACKGROUND
  Some anaesthetics exert an inhibitory effect on the response of the carotid body to low oxygen tension. However, the effect of dexmedetomidine on the carotid body response has not been reported.
  
  
  OBJECTIVE
  To investigate the effect of dexmedetomidine on carotid body activity. The hypothesis is that dexmedetomidine does not have an inhibitory effect on the response of the carotid body to low oxygen tension.
  
  
  METHODS
  Animal experimental study in vitro. Ten carotid bodies surgically removed from male New Zealand white rabbits were tested.
  
  
  METHODS
  Research laboratory of Nippon Medical School, Tokyo, Japan, from July 2008 to February 2010.
  
  
  METHODS
  The carotid body was perfused with three different concentrations of dexmedetomidine (0.1, 1.0 and 10 nmol l). The contribution of α2-adrenergic receptors was evaluated by addition of 1.0 nmol l yohimbine, an α2-adrenergic receptor antagonist.
  
  
  METHODS
  The differences in carotid sinus nerve activity between high oxygen tension (baseline) and low oxygen tension (peak) were analysed.
  
  
  RESULTS
  At all three concentrations, dexmedetomidine did not depress the baseline and peak activity of the carotid body, whereas 0.1 nmol l dexmedetomidine facilitated the response to low oxygen tension stimulation. The differences in carotid sinus nerve activity between baseline (pO2 80.4 ± 9.1 kPa) and peak (pO2 22.1 ± 2.6 kPa) were 140 ± 70 Hz in controls and 266 ± 116 Hz with 0.1 nM dexmedetomidine (P < 0.05). This increase was not shown in the presence of 1.0 nmol l yohimbine.
  
  
  CONCLUSIONS
  Dexmedetomidine does not depress the activity of the carotid body under high oxygen tension or the response to low oxygen tension, whereas 0.1 nmol l dexmedetomidine facilitates this response via α2-adrenergic receptor activation.
authors.affiliation: Department of Anesthesiology, Nippon Medical School, Tokyo, Japan. hidehiko123@gmail.com
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Nakatani
authors.forename: Chol
authors.initials: C
authors.lastname: Kim
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Sakamoto
mesh_terms: D000200:Action Potentials; D058647:Adrenergic alpha-2 Receptor Agonists / Q000494:pharmacology; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000777:Anesthetics / Q000494:pharmacology; D000818:Animals; D002344:Carotid Body / Q000187:drug effects / Q000378:metabolism*; D002346:Carotid Sinus / Q000187:drug effects; D020927:Dexmedetomidine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D008297:Male; D010100:Oxygen / Q000378:metabolism*; D011817:Rabbits; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D018712:Analgesics, Non-Narcotic; D000777:Anesthetics; D018341:Receptors, Adrenergic, alpha-2; D015016:Yohimbine; D020927:Dexmedetomidine; D010100:Oxygen