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• W2054310238 abstract "In Brief BACKGROUND: Many inhaled anesthetics inhibit voltage-gated sodium channels at clinically relevant concentrations, and suppression of neurotransmitter release by these anesthetics results, at least partly, from decreased presynaptic sodium channel activity. Volatile aromatic anesthetics can inhibit N-methyl-d-aspartate (NMDA) receptor function and enhance γ-amino butyric acid A receptor function, but these effects depend strongly on the chemical properties of the aromatic compounds. In the present study we tested whether diverse aromatic anesthetics consistently inhibit sodium channel function. METHODS: We studied the effect of eight aromatic anesthetics on Nav1.2 sodium channels with β1 subunits, using whole-cell, two-electrode voltage-clamp techniques in Xenopus oocytes. RESULTS: All aromatic anesthetics inhibited INa (sodium currents) at a holding potential which produce half-maximal current (V1/2) (partial depolarization); inhibition was modest with 1,3,5-trifluorobenzene (8% ± 2%), pentafluorobenzene (13% ± 2%), and hexafluorobenzene (13% ± 2%), but greater with benzene (37% ± 2%), fluorobenzene (39% ± 2%), 1,2-difluorobenzene (48% ± 2%), 1,4-difluorobenzene (31 ± 3%), and 1,2,4-trifluorobenzene (33% ± 1%). Such dichotomous effects were noted by others for NMDA and γ-aminobutyric acid A receptors. Parallel, but much smaller inhibition, was found for INa at a holding potential which produced near maximal current (−90 mV) (VH-90), and hexafluorobenzene caused small (6% ± 1%) enhancement of this current. These changes in sodium channel function were correlated with effectiveness for inhibiting NMDA receptors, with lipid solubility of the compounds, with molecular volume, and with cation-π interactions. CONCLUSION: Aromatic compounds vary in their actions on the kinetics of sodium channel gating and this may underlie their variable inhibition. The range of inhibition produced by minimum alveolar anesthetic concentration concentrations of inhaled anesthetics indicates that sodium channel inhibition may underlie the action of some of these anesthetics, but not others. IMPLICATIONS: Aromatic anesthetics can block N-methyl-d-aspartate receptors and enhance γ-aminobutyric acid A receptor responses. The present report finds various effects of these compounds on sodium channels. Although volatile aromatic anesthetics are not used clinically, exploring their effects on ion channels may aid in understanding the mechanisms of clinical inhaled anesthetic actions." @default.
• W2054310238 created "2016-06-24" @default.
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• W2054310238 date "2008-11-01" @default.
• W2054310238 modified "2023-10-14" @default.
• W2054310238 title "The Effects of Volatile Aromatic Anesthetics on Voltage-Gated Na+ Channels Expressed in Xenopus Oocytes" @default.
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• W2054310238 doi "https://doi.org/10.1213/ane.0b013e318184b966" @default.
• W2054310238 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2575119" @default.
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