Analgesic and Antihyperalgesic Properties of Propofol in a Human Pain Model

Bandschapp, Oliver; Filitz, Joerg; Ihmsen, Harald; Berset, Andreas; Urwyler, Albert; Koppert, Wolfgang; Ruppen, Wilhelm

doi:10.1097/aln.0b013e3181e33ac8

Cited by 82 publications

(79 citation statements)

References 43 publications

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“…This can be explained by the fact that the surgical insult was too weak to induce a clinically relevant effect, as sustained by the low peak levels of all inflammatory markers. The shorter length of stay in the recovery room after anesthesia with propofol is consistent with the recognized shorter anesthetic effect of propofol and our observation of lower pain ratings in the recovery room period in the propofol treated group confirms previous data [46][47][48][49].…”

Section: Propofolsupporting

confidence: 80%

Propofol and perioperative inflammation-the Intralipid® solvent may play a role

Bandschapp¹,

Chenaud²,

Inan³

et al. 2015

Glob Anesth Perioper Med

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The inflammatory properties of propofol are still debated. Apolipoprotein A-I is involved in the inflammation. We sought to determine how propofol or its solvent Intralipid® modulate Apolipoprotein A-I and the inflammatory response after surgical stress. Patients undergoing laparoscopic inguinal hernia repair were allocated to anesthesia with propofol (n=25), isoflurane alone (n=27) or in combination with Intralipid® (n=27). Apolipoprotein A-I and inflammation were assessed before, during and after surgery. Following a decrease in all groups, Apolipoprotein A-I levels tended to recover significantly earlier when propofol or Intralipid® were given (p<0.05). Cortisol increased in the control group whereas it remained at baseline levels when lipids were given. In this study the administration of lipids, i.e. propofol or its solvent Intralipid®, in the perioperative setting was associated with a more pronounced yet rapidly recovering acute phase reaction.

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Section: Propofolsupporting

confidence: 80%

Propofol and perioperative inflammation-the Intralipid® solvent may play a role

Bandschapp¹,

Chenaud²,

Inan³

et al. 2015

Glob Anesth Perioper Med

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“…[7,18] When propofol is used alone, higher doses are often required for gastrointestinal endoscopy because of its minimal analgesic activityand thus, deepening of sedation may occur. [9,[17][18][19][20][21][22] Thus, deepening in sedation may occur related to the propofol dose. [17,18-20-22] Oversedation resulting in hypoxemia was found to be responsible for most of the cardiac arrests.…”

Section: Discussionmentioning

confidence: 99%

Alternative sedation regimens for upper gastrointestinal endoscopy proven to be safe. A retrospective comparative study

Uzman

Gürbulak²,

Baltalı

et al. 2017

EJMO

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“…This effect is only local and occurring at high concentrations which has to be clearly differentiated of systemic effects at much lower concentrations. Propofol has an analgesic effect in subhypnotic concentrations (Hand et al, 2001;Bandschapp et al, 2010) and is able to suppress spinal sensitization (O'Connor and Abram, 1995) and interneuronal activity in cerebral cortex (Woodforth et al, 1999). However, the mechanisms underlying this analgesic effect remain unclear.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…However, the mechanisms underlying this analgesic effect remain unclear. A possible involvement of the peripheral nervous system has been discussed (Bandschapp et al, 2010) but no investigation so far was designed to look at the periphery. All the electrophysiological (clinical) investigations have so far considered the effect of general anaesthetics on afferent axons as negligible, since axons are not usually considered as neural targets for these agents (Raymond et al, 1991;Sloan and Jäntti, 2008).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

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Propofol decreases the axonal excitability in rat primary sensory afferents

et al. 2012

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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 A -fibres caused by propofol. Concentrations of 10 Mol, 100 Mol and 1000 Mol were tested. Latency, peak response, strength-duration time constant ( 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 Mol: 0.96±0.07ms; 1000 Mol 1.10±0.06ms, P<0.01). Also, propofol prolonged the relative refractory period (0 Mol: 1.79±1.13ms; 100 Mol: 2.53±1.38ms, P<0.01), and reduced superexcitability (0 Mol: -14.0±4.0%; 100 Mol: -9.5±5.5%) and subexcitability (0 Mol: 7.5±1.2%; 1000 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. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTThe 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 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 findings: Our results have shown that propofol decreases nerve excitability of rat primary sensory afferents in vitro. Latency increased with increasing concentrations (0 µMol: 0.96 ± 0.07 ms; 1000 µMol 1.10 ± 0.06 ms, P<0.01). Also, propofol prolonged the relative refractory period (0 µMol: 1.79 ± 1.13 ms; 100 µMol: 2.53 ± 1.38 ms, P<0.01), and reduced superexcitability (0 µMol: -14.0 ± 4.0%; 100 µMol: -9.5 ± 5.5 %) and subexcitability (0 µMol: 7.5 ± 1.2 %; 1000 µMol: 3.6 ± 1.2) significantly during the recovery cycle (P<0.01).Significance: Our results have shown that propofol decreases nerve exc...

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Analgesic and Antihyperalgesic Properties of Propofol in a Human Pain Model

Abstract: Propofol showed short-lasting analgesic properties during its administration, whereas the solvent-like formulation 10% Intralipid had no effect on pain perception.

Cited by 82 publications

References 43 publications

Propofol and perioperative inflammation-the Intralipid® solvent may play a role

Propofol and perioperative inflammation-the Intralipid® solvent may play a role

Alternative sedation regimens for upper gastrointestinal endoscopy proven to be safe. A retrospective comparative study

Propofol decreases the axonal excitability in rat primary sensory afferents

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