Effets électroencéphalographiques du sévoflurane à l’induction chez le jeune enfant : étude prospective sur 20 cas

Conreux, F.; Best, Olivier; Preckel, Marie-Pierre; Lhopitault, C; Beydon, L.; F, Pouplard; Granry, J.C.

doi:10.1016/s0750-7658(01)00393-8

Cited by 31 publications

(7 citation statements)

References 26 publications

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“…Many other studies report the occurrence of MES for sevoflurane concentrations higher than 1.5 MAC in epileptic adults, 24,25 healthy adults, [3][4][5][26][27][28] or healthy children. 2,18,19,29 Our results are consistent with that notion of "epileptogenic threshold" of approximately 1.5 MAC of sevoflurane. 23 Using the up-down progression we observed a clear stabilization of the crossover responses demonstrating that the occurrence of MES under sevoflurane could be a reproducible event.…”

Section: Discussionsupporting

confidence: 91%

“…However, as it has been previously suggested, 17 it is possible to make an approximate estimation of the number of patients necessary to achieve this goal, based on previous results. In our study, given the expected threshold of MES of approximately 4%, 2,5,18,19 the chosen FeSevo for the first patient (2.5% or 1 MAC), 16 and the incremental pace of 0.2%, we anticipated approximately 30 patients for group 1. For groups 2 and 3, because the FeSevo of the first patient was taken from the results of the first group, we expected only approximately 20 patients per group.…”

Section: Discussionmentioning

confidence: 99%

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Epileptogenic Effect of Sevoflurane

et al. 2012

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Epileptogenic Effect of Sevoflurane

et al. 2012

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“…It owes its popularity to its low airway irritability, ability to rapidly induce anesthesia and good pharmacokinetic performance (1)(2)(3). However, growing evidence demonstrates that sevoflurane caused severe side effects, particularly in infants (4,5). Indeed, sevoflurane was reported to induce high rates of postoperative cognitive dysfunction in comparison with other anesthetic agents (6).…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane‑induced neurotoxicity is driven by OXR1 post‑transcriptional downregulation involving hsa‑miR‑302e

et al. 2018

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Sevoflurane is a common anesthetic agent used in surgical settings and previous studies have indicated that it exerts a neurotoxic effect. However, the molecular mechanism underlying this side effect is unknown. In addition, the human microRNA‑302 (hsa‑miR‑302) family members have been reported to be involved in neuronal cell development and biology. Thus, the present study aimed to investigate the potential implication of hsa‑miR‑302e in the sevoflurane‑induced cytotoxicity on human hippocampal cells (HN‑h). HN‑h cells were transfected with hsa‑miR‑302e mimic, hsa‑miR‑302e inhibitor or negative controls and subsequently exposed to different concentrations of sevoflurane. An MTT assay was used to assess the cytotoxicity of sevoflurane on HN‑h cells. Cell apoptosis was determined by flow cytometry. The levels of lactate dehydrogenase release, reactive oxygen species, lipid peroxidation and intracellular calcium (Ca2+) were additionally detected. Reverse transcription‑quantitative polymerase chain reaction and western blotting were conducted to determine mRNA and protein expression, respectively. A luciferase assay was performed for validating the targeting of OXR1 by hsa‑miR‑302e. The results indicated that sevoflurane induced a decrease in cell viability, malondialdehyde and reactive oxygen species production, lactate dehydrogenase release, intracellular Ca2+ production, calcium/calmodulin‑dependent protein kinase II phosphorylation and apoptosis. In addition, treatment with sevoflurane induced the expression of hsa‑miR‑302e while the expression of its target, oxidation resistance gene 1 (OXR1), was significantly downregulated. Inhibition of hsa‑miR‑302e expression protected neuronal cells from sevoflurane cytotoxicity. Mechanistic studies demonstrated that OXR1 was a direct target of hsa‑miR‑302e. Furthermore, the overexpression of OXR1 abolished the effect of sevoflurane on neuronal cells. The results of the present study indicated that sevoflurane exerts its neurotoxic effect by regulating the hsa‑miR‑302e/OXR1 axis. Therefore, the manipulation of the hsa‑miR‑302e/OXR1 pathway will be useful for preventing sevoflurane‑induced neurotoxicity.

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“…No difference was found between the two groups in ETCO 2 , ETsevo, HR and PAM ( Table 2). The number of adjustments necessary to reach and maintain the target sevoflurane concentration was 1 (1-2.5[0-5]) in the TCII group and 6(5-6 [4][5][6][7][8][9][10]) in the control group (P < 0.0001). The mean sevoflurane consumption for induction was 20 (17-22.4[14.5-35.9]) ml in the TCII group, and could not be measured in the control group.…”

Section: Resultsmentioning

confidence: 99%