Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation

M. Orth, Linda S Barter, C. Dominguez, R. Atherley, Earl Carstens, J. F. Antognini

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Background. Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Methods. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8× or 1.2× the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED50) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Results. Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from ≈6 to ≈8.5 Hz, and the SEF from ≈25.5 to ≈27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED50 propofol, only the tail clamp and 1 Hz stimuli increased MEF (≈8 to ≈10-10.5 Hz). At the higher propofol infusion rate (1.2 ED50) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from ≈23 to ≈21.5 Hz). Conclusions. Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

Original languageEnglish (US)
Pages (from-to)477-484
Number of pages8
JournalBritish Journal of Anaesthesia
Volume95
Issue number4
DOIs
StatePublished - Oct 2005

Fingerprint

Propofol
Halothane
Tail
Anesthetics
Anesthesia
Unmyelinated Nerve Fibers
Constriction

Keywords

  • Anaesthetics i.v., propofol
  • Anaesthetics volatile, halothane
  • Brain, electroencephalography
  • Model, rat
  • Pain, experimental

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation. / Orth, M.; Barter, Linda S; Dominguez, C.; Atherley, R.; Carstens, Earl; Antognini, J. F.

In: British Journal of Anaesthesia, Vol. 95, No. 4, 10.2005, p. 477-484.

Research output: Contribution to journalArticle

Orth, M. ; Barter, Linda S ; Dominguez, C. ; Atherley, R. ; Carstens, Earl ; Antognini, J. F. / Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation. In: British Journal of Anaesthesia. 2005 ; Vol. 95, No. 4. pp. 477-484.
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abstract = "Background. Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Methods. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8× or 1.2× the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED50) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Results. Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from ≈6 to ≈8.5 Hz, and the SEF from ≈25.5 to ≈27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED50 propofol, only the tail clamp and 1 Hz stimuli increased MEF (≈8 to ≈10-10.5 Hz). At the higher propofol infusion rate (1.2 ED50) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from ≈23 to ≈21.5 Hz). Conclusions. Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.",
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T1 - Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation

AU - Orth, M.

AU - Barter, Linda S

AU - Dominguez, C.

AU - Atherley, R.

AU - Carstens, Earl

AU - Antognini, J. F.

PY - 2005/10

Y1 - 2005/10

N2 - Background. Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Methods. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8× or 1.2× the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED50) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Results. Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from ≈6 to ≈8.5 Hz, and the SEF from ≈25.5 to ≈27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED50 propofol, only the tail clamp and 1 Hz stimuli increased MEF (≈8 to ≈10-10.5 Hz). At the higher propofol infusion rate (1.2 ED50) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from ≈23 to ≈21.5 Hz). Conclusions. Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

AB - Background. Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Methods. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8× or 1.2× the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED50) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Results. Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from ≈6 to ≈8.5 Hz, and the SEF from ≈25.5 to ≈27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED50 propofol, only the tail clamp and 1 Hz stimuli increased MEF (≈8 to ≈10-10.5 Hz). At the higher propofol infusion rate (1.2 ED50) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from ≈23 to ≈21.5 Hz). Conclusions. Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

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