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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Anesthetics, Intravenous, Animals, Hypercapnia, Hypoglossal Nerve, Hypoxia, Male, Phrenic Nerve, Propofol, Rabbits, Respiration.
user
Does [ Propofol suppress the responses in hypoglossal nerve activity to hypercapnic-hypoxic stimulation ]? Context: 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. 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). 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.
assistant
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. Final Decision: yes