Investigation of the EEG effects of intravenous lidocaine during halothane anaesthesia in ponies

Murrell, Joanna C; White, Kate; Johnson, Craig B.; Taylor, Polly; Doherty, Thomas J; Waterman-Pearson, AE

doi:10.1111/j.1467-2995.2005.00201.x

Cited by 88 publications

(86 citation statements)

References 53 publications

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“…Significant increases in F50 and F95 were found during the first 10 s after decapitation. These are consistent with responses to noxious stimulation found in other studies 15,19,21,22 and can be interpreted as such. A significant and a gradual decrease in the Ptot was observed in the current study and was similar to the reductions in the power component of specific EEG frequency bands (1-100 Hz and 13-100 Hz) after decapitation of both conscious and anaesthetized rats reported in a recent study.…”

Section: Discussionsupporting

confidence: 81%

“…Similar changes in the EEG power spectrum in response to noxious stimulation have been demonstrated previously in a number of animal studies using the minimal halothane anaesthesia model. 14,15,[18][19][20] F50 and F95 of the EEG power spectrum increased significantly following decapitation of rats in the current study, but both these indices are independent of the total power of the EEG trace and so should be interpreted with caution in situations where Ptot is markedly reduced. In the present study, EEG remained active for a mean duration of 9.7 s, followed by a period of transitional EEG that proceeded to an isoelectric pattern by 15 s after decapitation.…”

Section: Discussionmentioning

confidence: 81%

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Electroencephalographic evaluation of decapitation of the anaesthetized rat

et al. 2013

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The objective of this study was to evaluate the changes in electroencephalographic (EEG) power spectrum in response to decapitation of anaesthetized rats, in order to assess the nociception or otherwise of this procedure. Ten young adult male Sprague-Dawley rats were anaesthetized with halothane in oxygen and anaesthesia was maintained at a stable concentration of halothane between 1.20% and 1.25%. The rat's head and neck were placed through the opening of a small animal guillotine so that the blade of the guillotine was positioned over the atlanto-occipial joint of the rat's neck. The EEG was recorded in a five-electrode montage, bilaterally. After recording a 15 min baseline the rat was decapitated by swiftly pressing the guillotine blade and the EEG recording was continued until the signal was isoelectric on both channels. Changes in the median frequency (F50), 95% spectral edge frequency (F95) and total power of the EEG (Ptot) were used to investigate the effects of decapitation. During the first 15 s following decapitation, there were significant increases in the F50 and F95, and a decrease in the Ptot compared with baseline values. There was a clear window of time immediately following decapitation where changes in the EEG frequency spectrum were obvious; these changes in the EEG indices of nociception could be attributed as responses generated by the rat's cerebral cortex following decapitation.Keywords rat, electroencephalogram, euthanasia, welfare, nociception Several different methods of euthanasia have been proposed for use in laboratory animals in biomedical research (e.g. injectable anaesthesia, decapitation, cervical dislocation, CO 2 asphyxiation, etc.). 1Decapitation has the advantage that it has no effect on subsequent analytical procedures.2 This is not the case with chemical methods such as a drug overdose. Despite its common use, the humaneness of decapitation of conscious animals is debatable.2-5 The question of whether brain activity continues after decapitation and, if so, for how long, has been considered essential for determining the acceptability of this procedure. These questions have been addressed in a number of studies involving different animal species including rats.2,6-10 Studies utilizing electroencephalographic (EEG) recordings have been used to map the brain following decapitation. Conversion from high voltage slow activity to low voltage fast activity (LVFA) and desynchronization, a shift in EEG activity toward high frequency, have been reported as typical EEG responses following the decapitation of conscious animals. These changes in EEG activity persist between 8 and 29 s in all species after decapitation 5 and, are followed by the onset of isoelectric EEG.Interpretation of these post-decapitation EEG changes in terms of conscious arousal and potential pain perception, and as a response to noxious stimulation, has not been simple. Other studies have demonstrated that LVFA pattern EEG activity can be seen during rapid eye movement sleep/anaesthesia and also during an...

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 81%

Electroencephalographic evaluation of decapitation of the anaesthetized rat

et al. 2013

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“…When compared with more traditional approaches to studies of potentially painful manipulations, this model has the advantage that a negative control group can be included without compromising the welfare of animals used in the study. It can also be used to compare the effectiveness of different analgesic regimens (Murrell et al 2002, Haga & Ranheim 2005, Johnson et al 2005, Murrell et al 2005.…”

mentioning

confidence: 99%

Comparative effects of halothane, isoflurane, sevoflurane and desflurane on the electroencephalogram of the rat

2008

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SummaryInhalant anaesthetic agents are commonly used in studies investigating the electroencephalographic (EEG) effects of noxious stimuli in animals. Halothane causes less EEG depression than isoflurane, however, the EEG effects of halothane, isoflurane, sevoflurane and desflurane have not been compared in the same model. This study aimed to compare the EEG effects of these inhalational agents in the rat.Forty male Sprague-Dawley rats were assigned to four groups and anaesthetized with halothane, isoflurane, sevoflurane or desflurane. EEG was recorded from the left and right somatosensory cortices for 5 min at three different multiples of minimal alveolar concentration (MAC) (1.25, 1.5 and 1.75). Median, 95% spectral edge frequency and total power were derived and a single mean value for each was calculated for the first 60 s of each recording period. When the raw EEG contained burst suppression (BS), the BS ratio (BSR) over 60 s was calculated. No BS was found in EEG recorded from the halothane group at any concentration. BS was present at all concentrations with the other anaesthetic agents. BS was almost complete at all concentrations of isoflurane, whereas BSR increased significantly with increasing concentrations of sevoflurane and desflurane. No significant differences were found between the BSR due to the 1.75 MAC multiple of isoflurane, sevoflurane or desflurane. Halothane causes significantly less depression of cortical activity than the newer inhalant agents at equivalent multiples of MAC. These data support the hypothesis that halothane has a fundamentally different mechanism of action than the other inhalant agents.

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“…32,78,[92][93][94][95] The drug must be administered as CRI due to its short half-life. 96 A loading dose of 1.3 to 1.5 mg/kg administered IV over 15 minutes (min) followed by a CRI of 50-100 µg•kg -1 •min -1 is most commonly used.…”

Section: Systemic Lidocainementioning

confidence: 99%

“…78,79 Data regarding the immediate analgesic effect of lidocaine on spontaneous (not evoked) pain in animals or patients are somewhat inconsistent when infused at clinically common doses, 78,91,97,98 and higher doses carry the risk of cardio-and neurotoxicity. 86,94 Since plasma concentrations achieved during long-term infusion vary widely among horses and may accumulate over time, 78,95,96,100,101 monitoring of plasma levels (via a lidocaine ELISA kit; Neogen Corporation, Lansing, MI 48912, USA) is recommended, not only to avoid toxicity but also to ensure that analgesically effective concentrations (approx. ≥ 1 µg/mL) 91,95 are being achieved.…”

Section: Systemic Lidocainementioning

confidence: 99%