• Nobuo Umezawa, Hirofumi Arisaka, Shigeki Sakuraba, Takeo Sugita, Akiko Matsumoto, Yuki Kaku, Kazu-ichi Yoshida, and Shun-ichi Kuwana.
• Department of Anesthesiology, Kanagawa Dental University, Yokosuka City 238-8580, Japan.
• Respir Physiol Neurobiol. 2015 Jan 1;205:61-5.

AbstractOrexins (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.Copyright © 2014 Elsevier B.V. All rights reserved.

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