Pronounced depression by propofol on carotid body response to CO2 and K+ -induced carotid body activation

Abstract Propofol is a commonly used anesthetic agent, and it attenuates hypoxic ventilatory response in humans. Propofol reduce in vivo and in vitro carotid body responses to hypoxia as well as to nicotine in experimental animals. In the present study we examined the effects of propofol on carotid...

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Bibliographic Details
Published in:Respiratory physiology & neurobiology 2008-02, Vol.160 (3), p.284-288
Main Authors: Akada, Shingi, Fagerlund, Malin Jonsson, Lindahl, Sten G.E, Sakamoto, Atsuhiro, Prabhakar, Nanduri R, Eriksson, Lars I
Format: Article
Language:English
Subjects:
Action Potentials - drug effects
Analysis of Variance
Anesthetics, Intravenous - pharmacology
Anesthetics. Neuromuscular blocking agents
Animals
Biological and medical sciences
Carotid Body - drug effects
Carotid Body - metabolism
Chemoreceptor Cells - drug effects
Chemoreceptor Cells - physiology
Hypercapnia - pathology
Hypercapnia - physiopathology
In Vitro Techniques
Medical Education
Medical sciences
Medicin och hälsovetenskap
Neuropharmacology
Pharmacology. Drug treatments
Potassium - pharmacology
Propofol - pharmacology
Pulmonary/Respiratory
Rabbits
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Summary:Abstract Propofol is a commonly used anesthetic agent, and it attenuates hypoxic ventilatory response in humans. Propofol reduce in vivo and in vitro carotid body responses to hypoxia as well as to nicotine in experimental animals. In the present study we examined the effects of propofol on carotid body responses to hypercapnia and K+ -induced carotid body activation and compared these effects with hypoxia in an in vitro rabbit carotid body preparation. Hypoxia, hypercapnia and potassium increased the carotid sinus nerve activity and propofol attenuated the chemoreceptor responses to all three stimuli. However, the magnitude of propofol-induced attenuation was greater for hypercapnic and K+ -induced carotid body activation compared to the hypoxic response. These observations suggest that propofol-induced attenuation of the hypoxic response is partly secondary to depression of chemoreceptor response to hypercapnia inhibiting the synergistic interactions between O2 and CO2 and may involve CO2 /H+ sensitive K+ channels.
ISSN:1569-9048
1878-1519
DOI:10.1016/j.resp.2007.10.011