Target concentration of propofol required to insert the laryngeal mask airway in children

Viviand, X.; Berdugo, L.; Noë, C Aubry de la; Lando, A.; Martin, Claude

doi:10.1046/j.1460-9592.2003.01006.x

Cited by 14 publications

(9 citation statements)

References 19 publications

(35 reference statements)

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“…Anesthesiologists commonly encounter airway complications during LMA insertion such as coughing, gagging, hiccups, or aspiration [15]. However, the LMA can be inserted smoothly after suppression of airway reflexes with adequate anesthesia [16].…”

Section: Discussionmentioning

confidence: 99%

Optimal conditions for Laryngeal Mask Airway insertion in children can be determined by the trapezius squeezing test

Chang

Shim

Shin

et al. 2008

Journal of Clinical Anesthesia

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Section: Discussionmentioning

confidence: 99%

Optimal conditions for Laryngeal Mask Airway insertion in children can be determined by the trapezius squeezing test

Chang

Shim

Shin

et al. 2008

Journal of Clinical Anesthesia

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“…25–27 Propofol is a highly lipophilic agent and therefore the concentration of propofol is relatively high (22–112 μM/4–20 μg/ml) in lipid-rich tissues such as the brain. 28–32 Different doses of propofol have been reported to induce neurotoxicity.…”

Section: Methodsmentioning

confidence: 99%

Insufficient Astrocyte-Derived Brain-Derived Neurotrophic Factor Contributes to Propofol-Induced Neuron Death Through Akt/Glycogen Synthase Kinase 3β/Mitochondrial Fission Pathway

Liu

Yan²,

Inagaki³

et al. 2017

Anesthesia &Amp; Analgesia

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BACKGROUND Growing animal evidence demonstrates that prolonged exposure to propofol during brain development induces widespread neuronal cell death, but there is little information on the role of astrocytes. Astrocytes can release neurotropic growth factors such as brain-derived neurotropic factor (BDNF), which can exert the protective effect on neurons in paracrine fashion. We hypothesize that during propofol anesthesia, BDNF released from developing astrocytes may not be sufficient to prevent propofol-induced neurotoxicity. METHODS Hippocampal astrocytes and neurons isolated from neonatal Sprague Dawley rats were exposed to propofol at a clinically relevant dose of 30 μM or dimethyl sulfoxide as control for 6 h. Propofol-induced cell death was determined by propidium iodide (PI) staining in astrocyte-alone cultures, neuron-alone cultures, or co-cultures containing either low or high density of astrocytes [1:9 or 1:1 ratio of astrocytes to neurons (ANR), respectively)]. The astrocyte-conditioned medium was collected 12 h following propofol exposure and measured by protein array assay. BDNF concentration in astrocyte-conditioned medium was quantified using ELISA. Neuron-alone cultures were treated with BDNF, tyrosine receptor kinase B (TrkB) inhibitor Cyclotraxin-B, glycogen synthase kinase 3β (GSK3β) inhibitor CHIR99021, or mitochondrial fission inhibitor Mdivi-1 prior to propofol exposure. Western blot was performed for quantification of the level of Akt and GSK3β. Mitochondrial shape was visualized through TOM20 staining. RESULTS Propofol increased cell death in neurons by 1.8 fold [% of PI-positive cells (PI%) =18.6, 95% CI=15.2–21.9, P<0.05], but did not influence astrocyte viability. The neuronal death was attenuated by a high ANR (1:1 co-cultures) [fold change (FC) =1.17, 95% CI=0.96–1.38, P<0.05), but not with a low ANR (1:9 co-cultures)] (FC=1.87, 95% CI=1.48–2.26, P>0.05). Astrocytes secreted BDNF in a cell density-dependent way and propofol decreased BDNF secretion from astrocytes. Administration of BDNF, CHIR99021, or Mdivi-1 significantly attenuated the propofol-induced neuronal death and aberrant mitochondria in neuron-alone cultures (FC=0.8, 95% CI=0.62–0.98; FC=1.22, 95% CI=1.11–1.32; FC=1.35, 95% CI=1.16–1.54 respectively, P<0.05) and the co-cultures with a low ANR (1:9) (FC=0.85, 95% CI=0.74–0.97; FC=1.08, 95% CI=0.84–1.32; FC=1.25, 95% CI=1.1–1.39 respectively, P<0.05) Blocking BDNF receptor or Akt activity abolished astrocyte-induced neuroprotection in the co-cultures with a high ANR (1:1). CONCLUSIONS Astrocytes attenuate propofol-induced neurotoxicity through BDNF-mediated cell survival pathway suggesting multiple neuroprotective strategies such as administration of BDNF, astrocyte-conditioned medium, decreasing mitochondrial fission, or inhibition of GSK3β.

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“…31–34 The dose of propofol used clinically in children varies widely but typically ranges from about 1–10 μg/mL (blood concentration) with higher doses used for induction of anesthesia and lower doses used for maintenance. 35–37 In addition, cell culture and whole animal studies have shown that propofol can induce toxicity at high doses or prolonged exposure times after a single exposure. 5,31,38,39 Thus, 2-week-old hESC-derived neurons were treated with 0, 5, 10 and 20 μg/mL of research grade propofol (0–112 μM, Sigma-Aldrich) or equal volume of dimethyl sulfoxide (DMSO, Sigma-Aldrich) as the vehicle control in 60 mm culture dishes (500,000 cells/dish) or 12 mm glass coverslips (100,000 cells/coverslip).…”

Section: Methodsmentioning

confidence: 99%

Down-regulation of MicroRNA-21 Is Involved in the Propofol-induced Neurotoxicity Observed in Human Stem Cell–derived Neurons

Twaroski

Yan²,

Olson³

et al. 2014

Anesthesiology

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Background Recent studies in various animal models have suggested that anesthetics such as propofol, when administered early in life, can lead to neurotoxicity. These studies have raised significant safety concerns regarding the use of anesthetics in the pediatric population and highlight the need for a better model by which to study anesthetic-induced neurotoxicity in humans. Human embryonic stem cells (hESCs) are capable of differentiating into any cell type and represent a promising model to study mechanisms governing anesthetic-induced neurotoxicity. Methods Cell death in hESC-derived neurons was assessed using TUNEL staining and microRNA (miR) expression was assessed using quantitative reverse transcription polymerase chain reaction (qRTPCR). miR-21 was overexpressed and knocked down using a miR-21 mimic and antagomir, respectively. Sprouty 2 was knocked down using a small interfering RNA and the expression of the miR-21 targets of interest was assessed by Western blot. Results Propofol dose and exposure time-dependently induced significant cell death (n = 3) in the neurons and downregulated several microRNAs, including miR-21. Overexpression of miR-21 and knockdown of Sprouty 2 attenuated the increase in TUNEL-positive cells following propofol exposure. In addition, miR-21 knockdown increased the number of TUNEL-positive cells by 30% (n = 5). Finally, activated Signal Transducer and Activator of Transcription 3 (STAT3) and protein kinase B (Akt) were downregulated and Sprouty 2 was upregulated following propofol exposure (n = 3). Conclusions These data suggest that: (1) hESC-derived neurons represent a promising in vitro human model for studying anesthetic-induced neurotoxicity, (2) propofol induces cell death in hESC-derived neurons and (3) the propofol-induced cell death may occur via a STAT3/miR-21/Sprouty2-dependent mechanism.

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Target concentration of propofol required to insert the laryngeal mask airway in children

Abstract: The target-controlled infusion technique for anaesthesia induction and insertion of the LMA was a safe and effective technique in our study.

Cited by 14 publications

References 19 publications

Optimal conditions for Laryngeal Mask Airway insertion in children can be determined by the trapezius squeezing test

Optimal conditions for Laryngeal Mask Airway insertion in children can be determined by the trapezius squeezing test

Insufficient Astrocyte-Derived Brain-Derived Neurotrophic Factor Contributes to Propofol-Induced Neuron Death Through Akt/Glycogen Synthase Kinase 3β/Mitochondrial Fission Pathway

Down-regulation of MicroRNA-21 Is Involved in the Propofol-induced Neurotoxicity Observed in Human Stem Cell–derived Neurons

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