• Lisa Neukom, Nisha Vastani, Burkhardt Seifert, Donat R Spahn, and Konrad Maurer.
• Institute of Anesthesiology, University Hospital of Zurich, Switzerland.
• Life Sci. 2012 Feb 27;90(9-10):343-50.

AimsThe aim of this present study was to investigate the changes of peripheral sensory nerve excitability produced by propofol.Main MethodsIn a recently described in vitro model of rodent saphenous nerve we used the technique of threshold tracking (QTRAC®) to measure changes of axonal nerve excitability of Aβ-fibres caused by propofol. Concentrations of 10 μMol, 100 μMol and 1000 μMol were tested. Latency, peak response, strength-duration time constant (τSD) and recovery cycle of the sensory neuronal action potential (SNAP) were recorded.Key FindingsOur results have shown that propofol decreases nerve excitability of rat primary sensory afferents in vitro. Latency increased with increasing concentrations (0μMol: 0.96 ± 0.07ms; 1000μMol 1.10 ± 0.06ms, P<0.01). Also, propofol prolonged the relative refractory period (0μMol: 1.79 ± 1.13ms; 100 μMol: 2.53 ± 1.38ms, P<0.01), and reduced superexcitability (0 μMol: -14.0±4.0%; 100μMol: -9.5 ± 5.5%) and subexcitability (0μMol: 7.5 ± 1.2%; 1000μMol: 3.6 ± 1.2) significantly during the recovery cycle (P<0.01).SignificanceOur results have shown that propofol decreases nerve excitability of primary sensory afferents. The technique of threshold tracking revealed that axonal voltage-gated ion channels are significantly affected by propofol and therefore might be at least partially responsible for earlier described analgesic effects.Copyright © 2011 Elsevier Inc. All rights reserved.

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