Orexin-B antagonized respiratory depression induced by sevoflurane, propofol, and remifentanil in isolated brainstem-spinal cords of neonatal rats

Abstract Orexins (hypocretins) play a crucial role in arousal, feeding, and endocrine function. We previously reported that orexin-B activated respiratory neurons in the isolated brainstem-spinal cords of neonatal rats. We herein determined whether orexin-B antagonized respiratory depression induced...

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Published in:Respiratory physiology & neurobiology 2015-01, Vol.205, p.61-65
Main Authors: Umezawa, Nobuo, Arisaka, Hirofumi, Sakuraba, Shigeki, Sugita, Takeo, Matsumoto, Akiko, Kaku, Yuki, Yoshida, Kazu-ichi, Kuwana, Shun-ichi
Format: Article
Language:English
Subjects:
Anesthetics
Anesthetics - pharmacology
Animals
Animals, Newborn
Brain Stem - drug effects
Disease Models, Animal
Intracellular Signaling Peptides and Proteins - pharmacology
Isolated brainstem
Medical Education
Methyl Ethers - pharmacology
Neontal rat
Neuropeptides - pharmacology
Orexin
Orexins
Piperidines - pharmacology
Propofol - pharmacology
Pulmonary/Respiratory
Rats
Rats, Wistar
Respiration
Respiratory Insufficiency - chemically induced
Respiratory Insufficiency - prevention & control
Spinal Cord - drug effects
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Summary:Abstract Orexins (hypocretins) play a crucial role in arousal, feeding, and endocrine function. We previously reported that orexin-B activated respiratory neurons in the isolated brainstem-spinal cords of neonatal rats. We herein determined whether orexin-B antagonized respiratory depression induced by sevoflurane, propofol, or remifentanil. We recorded C4 nerve bursts as an index of inspiratory activity in a brainstem-spinal cord preparation. The preparation was superfused with a solution equilibrated with 3% sevoflurane alone for 10 min and the superfusate was then switched to a solution containing sevoflurane plus orexin-B. Sevoflurane decreased the C4 burst rate and the integrated C4 amplitude. The C4 burst rate and amplitude were reversed by 0.5 μM orexin-B, but not by 0.1 μM orexin-B. The decrease induced in the C4 burst rate by 10 μM propofol or 0.01 μM remifentanil was significantly antagonized by 0.1 μM orexin-B. Respiratory depression induced by a higher concentration (0.1 μM) of remifentanil was not restored by 0.1 μM orexin-B. These results demonstrated that orexin-B antagonized respiratory depression induced by sevoflurane, propofol, or remifentanil.
ISSN:1569-9048
1878-1519
DOI:10.1016/j.resp.2014.10.013