title: [Propofol suppresses the responses in hypoglossal nerve activity to hypercapnic-hypoxic stimulation].
abstract: BACKGROUND
  Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by propofol. To estimate the influence of propofol (PP) on respiratory control, we studied its effect on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) manifesting in the hypoglossal nerve (HG) and the phrenic nerve (PN) in rabbits.
  
  
  METHODS
  Experiments were performed on adult rabbits vagotomized, paralyzed and ventilated artificially with 50% N2O, 50% oxygen and 0.5% sevoflurane. We evaluated and compared the effects of PP on the peak amplitude (AMP) and the root mean square (RMS) of HG and PH, and respiratory cycle (Tc).
  
  
  RESULTS
  PP depressed HG activity more than PH activity, and increased Tc in a dose related manner, with 0.25 mg x kg(-1) x min(-1) continuous infusion, propofol soon began to reduce both AMPs without any remarkable changing in Tc. AMP&RMS-HG were reduced to about 35% and AMP&RMS-PN to 80% of control. Administration of propofol 1.5 mg x kg(-1) x min(-1) vanished the activity of HG in all animals. RA made a mixed hypercapnic and hypoxic condition and induced RA response which was characterized by raised AMPs, augmented RMSs (deltaAMPs, deltaRMSs) in activity of both nerves activity and lengthened Tc (deltaTc). PP depressed RA response in HG dose-dependently, but did not do so in PN. Significant depressions in cardiovascular effects with tested dosage of PP occurred, but the values were kept in physiological ranges.
  
  
  CONCLUSIONS
  These results suggest that propofol induces respiratory depression by its inhibitory effect on the neural regulation of respiration, especially on the maintenance system of upper airway patency and the reflex related to the chemosensitive upper airway patency control.
authors.affiliation: Department of Anesthesiology, Saitama Medical School, Saitama 350-0495.
authors.forename: Shinichi
authors.initials: S
authors.lastname: Nakamura
authors.forename: Rie
authors.initials: R
authors.lastname: Ohno
authors.forename: Masahiko
authors.initials: M
authors.lastname: Suzuki
authors.forename: Taeko
authors.initials: T
authors.lastname: Abe
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Narita
authors.forename: Go
authors.initials: G
authors.lastname: Kusumoto
authors.forename: Masahiko
authors.initials: M
authors.lastname: Tsuchiya
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mizumoto
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Murakami
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagasaka
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Miyata
mesh_terms: D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D006935:Hypercapnia / Q000503:physiopathology*; D007002:Hypoglossal Nerve / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D010791:Phrenic Nerve / Q000502:physiology*; D015742:Propofol / Q000494:pharmacology*; D011817:Rabbits; D012119:Respiration
chemical_list: D018686:Anesthetics, Intravenous; D015742:Propofol