J Anesth Perioper Med. 2015;2(1):1-7. https://doi.org/10.24015/ebcmed.japm.2015.0001

Comparison of Spinal Anesthetic Effect between Emulsified Isoflurane and Emulsified Nonimmobilizer F6

Jiao Guo1,2*, Cheng Zhou1*, Peng Liang2, Xiao-jia Wang1,2, Yi Zhao1,2, and Jin Liu1,2

From the 1Laboratory of Anesthesia & Critical Care Medicine, 2Department of Anesthesiology, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.

*Jiao Guo and Cheng Zhou contributed equally to this study.

Correspondence to Dr. Cheng Zhou at zhouc@163.com and Dr. Jin Liu at scujinliu@foxmail.com.

EBCMED ID: ebcmed.japm.2015.0001 DOI: 10.24015/ebcmed.japm.2015.0001


Abstract

Background
Our previous study found that emulsified isoflurane (EI) produced subarachnoid anesthesia in dogs. The spinal effect of isoflurane might account for its immobility action. 1, 2-dichlorohexafluorocyclobutane (F6) is a nonimmobilizer that is incapable of causing immobility, it is therefore interesting to know whether there are different spinal anesthetic actions between emulsified F6 and isoflurane and their underlying mechanisms.

Methods
EI and emulsified F6 were intrathecally injected into rats, and motor and sensory functions were evaluated. Sodium channel currents were recorded from spinal neurons. The effect of EI and emulsified F6 on sodium channel was examined.

Results
EI produced subarachnoid anesthesia (median effective concentration [EC50] at 3.65%). Duration of actions of 8% EI was similar to 1% lidocaine. Emulsified F6 did not produce spinal anesthesia at 2% (5 folds of its predicted EC50). Meanwhile, EI inhibited sodium channel currents with median inhibitory concentration (IC50) at 0.81 ± 0.09 mmol/L and hyperpolarized voltage-dependent inactivation of sodium channel (from -57.5±2.4 to -66.3±1.8 mV, P<0.01). Emulsified F6 slightly inhibited sodium channel currents and no effect was found to the channel gating.

Conclusions
Neither spinal anesthetic action nor effect to sodium channel was observed for nonimmobilizer F6, while EI inhibited spinal neurons sodium channels at clinically relevant concentrations and produced spinal anesthesia.

Article Type
Original Article

Declaration of Interests
The authors declare no other competing interests.

Acknowledgements
This work was supported by the grant 2014M552361 (to Dr. Cheng Zhou) from the National Postdoctoral Foundation of China and the grant 81401139 (to Dr. Cheng Zhou) from the National Natural Science Foundation of China.

This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.