Comparison of TIVA with different combinations of ketamine–propofol mixtures in pediatric patients

Biricik, Ebru; Karacaer, Feride; Güleç, Ersel; Sürmelioğlu, Özgür; Ilgınel, Murat Türkeün; Özcengiz, Dilek

doi:10.1007/s00540-017-2438-8

Cited by 12 publications

(13 citation statements)

References 32 publications

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“…Propofol (2,6-diisopropylphenol) has been commonly used in pediatric and obstetric patients as an intravenous anesthetic and sedative drug because of its rapid onset, continuous infusion without accumulation and quick recovery 1,2. However, fetal and neonatal exposure to antagonists for N-methyl-D-aspartate (NMDA) receptors or agonists for γ-aminobutyric acid (GABA) receptors may lead to accelerated neurodegeneration 3.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway

Xiao

Zhou

et al. 2018

NDT

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BackgroundPropofol induces short- and long-term neurotoxicity. Our previous study showed that dexmedetomidine (Dex) can attenuate the propofol-induced acute neurotoxicity in rodents by enhancing the PI3K/Akt signaling. However, whether treatment of young rats with Dex could protect them from long-term neurotoxicity induced by propofol is unclear.Materials and methodsSeven-day-old male Sprague Dawley rats were randomized and injected intraperitoneally with saline (100 μL, NS), propofol (100 mg/kg), Dex (75 μg/kg), propofol (100 mg/kg) plus Dex (25, 50 or 75 μg/kg), 10% dimethyl sulfoxide (DMSO, 100 μL) or TDZD-8 (a GSK3β inhibitor, 1 mg/kg), or intracerebroventricularly with DMSO (5 μL) or LY294002 (a PI3K inhibitor, 25 μg/5 μL DMSO). Other rats in the experimental group were injected with the same doses of propofol, Dex and LY294002 or TDZD-8. All the rats were monitored until they were 9 weeks old. Their spatial learning and memory were tested by Morris water maze. The neuronal apoptosis, expression of PSD95, expression and phosphorylation of Akt and GSK3β and synaptic ultrastructures were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, immunohistochemistry, Western blot and transmission electron microscopy assays, respectively.ResultsCompared with the NS control group, young rats injected with intralipid, Dex, TDZD-8, LY294002 or DMSO alone did not show any significant change as they aged. Propofol significantly increased the escape latency time, hippocampal neuroapoptosis and synaptic ultrastructural changes but decreased the relative levels of PSD95 expression, and Akt and GSK3β phosphorylation in the developing hippocampus of the rats. The neuronal toxic effects of propofol were significantly mitigated by the pretreatment with a higher dose of Dex. The neuroprotective effect of Dex was enhanced by the treatment with TDZD-8, but was completely abrogated by the treatment with LY294002.ConclusionOur results indicated that the pretreatment of young rats with Dex attenuated the propofol-induced long-term neurotoxicity in their developing hippocampus by enhancing the PI3K/Akt signaling.

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Section: Introductionmentioning

confidence: 99%

Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway

Xiao

Zhou

et al. 2018

NDT

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“…There is no evidence that propofol induces neurotoxicity in humans [27], and the propofol related lypid syndrome, that is more likely to appear in pediatric population, occurs in high doses exceeding 4 mg/bw/h administered for over 24 hours [28]. Younger children are more resistant to the respiratory depressant effects of the Propofol and special care for children with associated autoimmune disorders is needed [29] Propofol is the most effective drug for intravenous monitored anesthesia care sedation in children undergoing spinal anesthesia [30].…”

Section: Resultsmentioning

confidence: 99%

Effect of 2,6-diisopropylphenol and 1,1,1,3,3,3-hexafluoro-2-(fluoromethoxy) propane as Anesthetic

Lupu¹,

Miulescu²,

Ștefanopol³

et al. 2019

Rev. Chim.

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Sevoflurane (2,2,2-trifluoro-1-[trifluoromethyl]ethyl fluoromethyl ether or C4H3F7O), with a molar mass 200.055 g/mol, also called fluoromethyl, is a highly fluorinated methyl isopropyl ether with general anesthetic property, available for clinical practice for about 30 years. Sevoflurane is a sweet-smelling, non-flammable and it is used for induction and maintenance of general anesthesia. Together with desflurane, it is replacing isoflurane and halothane in modern anesthesiology. Propofol (2,6-diisopropylphenol or C12H18O), with a molar mass 178.271g/mol is an alkylphenol derivative formulated for induction and maintenance (in some cases) of general anesthesia, sedation and hypnosis and acting as an intravenous anaesthetic drug, having largely replaced sodium thiopental because recovery from propofol is more rapid and clear.

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“…For total intravenous anesthesia in pediatric patients [25], remimazolam might be preferable because of less injection pain and no risk of propofol infusion syndrome. Propofol has an advantage to reduce laryngospasm and airway reactivity [26] but midazolam rarely cause laryngospasm [27].…”

Section: Pediatric Anesthesiamentioning

confidence: 99%

Remimazolam besilate, a benzodiazepine, has been approved for general anesthesia!!

Masui

2020

J Anesth

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Comparison of TIVA with different combinations of ketamine–propofol mixtures in pediatric patients

Abstract: ClinicalTrials.gov identifier: NCT02848963.

Cited by 12 publications

References 32 publications

Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway

Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway

Effect of 2,6-diisopropylphenol and 1,1,1,3,3,3-hexafluoro-2-(fluoromethoxy) propane as Anesthetic

Remimazolam besilate, a benzodiazepine, has been approved for general anesthesia!!

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