| LIFE SCIENCES | 卷:90 |
| Propofol decreases the axonal excitability in rat primary sensory afferents | |
| Article | |
| Seifert, Burkhardt2  Maurer, Konrad1,3,4  | |
| [1] Univ Zurich Hosp, Inst Anesthesiol, Pain Res Unit, CH-8091 Zurich, Switzerland | |
| [2] Univ Zurich, Inst Social & Prevent Med, Biostat Unit, CH-8006 Zurich, Switzerland | |
| [3] Univ Zurich, Inst Physiol, CH-8006 Zurich, Switzerland | |
| [4] Univ Zurich, Zurich Ctr Integrat Human Physiol ZIHP, CH-8006 Zurich, Switzerland | |
| 关键词: Propofol; Nerve excitability; Sensory afferents; Threshold tracking; | |
| DOI : 10.1016/j.lfs.2011.12.007 | |
| 来源: Elsevier | |
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【 摘 要 】
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 (R)) to measure changes of axonal nerve excitability of A beta-fibres caused by propofol. Concentrations of 10 mu Mol, 100 mu Mol and 1000 mu Mol were tested. Latency, peak response, strength-duration time constant (tau SD) 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 (0 mu Mol: 0.96 +/- 0.07 ms; 1000 mu Mol 1.10 +/- 0.06 ms, P<0.01). Also, propofol prolonged the relative refractory period (0 mu Mol: 1.79 +/- 1.13 ms; 100 mu Mol: 2.53 +/- 1.38 ms, P<0.01), and reduced superexcitability (0 mu Mol: 14.0 +/- 4.0%; 100 mu Mol: -9.5 +/- 5.5%) and subexcitability (0 mu Mol: 7.5 +/- 1.2%; 1000 mu Mol: 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. (C) 2011 Elsevier Inc. All rights reserved.
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| 10_1016_j_lfs_2011_12_007.pdf | 360KB |
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