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Propofol decreases the axonal excitability in rat primary sensory afferents


Neukom, Lisa; Vastani, Nisha; Seifert, Burkhardt; Spahn, Donat R; Maurer, Konrad (2012). Propofol decreases the axonal excitability in rat primary sensory afferents. Life Sciences, 90(9-10):343-350.

Abstract

AIMS: The aim of this present study was to investigate the changes of peripheral sensory nerve excitability produced by propofol. MAIN METHODS: In 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 10μMol, 100μMol and 1000μMol were tested. Latency, peak response, strength-duration time constant (τSD) and recovery cycle of the sensory neuronal action potential (SNAP) were recorded. KEY FINDINGS: Our 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; 100μMol: 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). SIGNIFICANCE: Our 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.

AIMS: The aim of this present study was to investigate the changes of peripheral sensory nerve excitability produced by propofol. MAIN METHODS: In 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 10μMol, 100μMol and 1000μMol were tested. Latency, peak response, strength-duration time constant (τSD) and recovery cycle of the sensory neuronal action potential (SNAP) were recorded. KEY FINDINGS: Our 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; 100μMol: 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). SIGNIFICANCE: Our 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.

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3 citations in Web of Science®
3 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Epidemiology, Biostatistics and Prevention Institute (EBPI)
04 Faculty of Medicine > University Hospital Zurich > Institute of Anesthesiology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2012
Deposited On:15 Jan 2012 17:33
Last Modified:05 Apr 2016 15:23
Publisher:Elsevier
ISSN:0024-3205
Publisher DOI:10.1016/j.lfs.2011.12.007
PubMed ID:22227474
Permanent URL: http://doi.org/10.5167/uzh-55136

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