ArticleAnesthesiology2015
Brain maturation in neonatal rodents is impeded by sevoflurane anesthesia.
Article in Anesthesiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 36 citations in OpenAlex.
- Comparison of Cognitive Deterioration Between Propofol and Remimazolam Anesthesia in ApoE4 Knock-In Mouse Model.International journal of molecular sciences · 2025Article
- Article
- Comparative study of the effects of prenatal sevoflurane exposure at different cortical stages on forebrain development and maturation in offspring.Frontiers in neuroscience · 2025Article
- Pre-adolescence repeat exposure to sub-anesthetic doses of ketamine induces long-lasting behaviors and cognition impairment in male and female rat adults.IBRO neuroscience reports · 2024Article
- Differential Effects of Sevoflurane Exposure on Long-Term Fear Memory in Neonatal and Adult Rats.Molecular neurobiology · 2022Article
- LncRNA Riken Attenuated Sevoflurane-Induced Neuroinflammation by Regulating the MicroRNA-101a/MKP-1/JNK Pathway.Neurotoxicity research · 2022Article
- Resveratrol ameliorates neuronal apoptosis and cognitive impairment by activating the SIRT1/RhoA pathway in rats after anesthesia with sevoflurane.Bosnian journal of basic medical sciences · 2022Article
- Sevoflurane promotes premature differentiation of dopaminergic neurons in hiPSC-derived midbrain organoids.Frontiers in cell and developmental biology · 2022Article
- Propofol and Sevoflurane Anesthesia in Early Childhood Do Not Influence Seizure Threshold in Adult Rats.International journal of environmental research and public health · 2021Article
- Surgery requiring general anesthesia in preterm infants is associated with altered brain volumes at term equivalent age and neurodevelopmental impairment.Pediatric research · 2021Observational
- Neonatal sevoflurane exposure induces impulsive behavioral deficit through disrupting excitatory neurons in the medial prefrontal cortex in mice.Translational psychiatry · 2020Article
- Sevoflurane Exposure Induces Neuronal Cell Parthanatos Initiated by DNA Damage in the Developing Brain via an Increase of Intracellular Reactive Oxygen Species.Frontiers in cellular neuroscience · 2020Article
- Cistanches alleviates sevoflurane-induced cognitive dysfunction by regulating PPAR-γ-dependent antioxidant and anti-inflammatory in rats.Journal of cellular and molecular medicine · 2020Article
- Noninvasive Tracking of Anesthesia Neurotoxicity in the Developing Rodent Brain.Anesthesiology · 2018Article
- Sevoflurane Affects Oxidative Stress and Alters Apoptosis Status in Children and Cultured Neural Stem Cells.Neurotoxicity research · 2018Article
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8 authors at 1 institution in 2 countries.
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Abstract
backgroundA wealth of data shows neuronal demise after general anesthesia in the very young rodent brain. Herein, the authors apply proton magnetic resonance spectroscopy (1HMRS), testing the hypothesis that neurotoxic exposure during peak synaptogenesis can be tracked via changes in neuronal metabolites.
methods1HMRS spectra were acquired in the brain (thalamus) of neonatal rat pups 24 and 48 h after sevoflurane exposure on postnatal day (PND) 7 and 15 and in unexposed, sham controls. A repeated measure ANOVA was performed to examine whether changes in metabolites were different between exposed and unexposed groups. Sevoflurane-induced neurotoxicity on PND7 was confirmed by immunohistochemistry.
resultsIn unexposed PND7 pups (N = 21), concentration of N-acetylaspartate (NAA; [NAA]) increased by 16% from PND8 to PND9, whereas in exposed PND7 pups (N = 19), [NAA] did not change and concentration of glycerophosphorylcholine and phosphorylcholine ([GPC + PCh]) decreased by 25%. In PND15 rats, [NAA] increased from PND16 to PND17 for both the exposed (N = 14) and the unexposed (N = 16) groups. Two-way ANOVA for PND7 pups demonstrated that changes over time observed in [NAA] (P = 0.031) and [GPC + PCh] (P = 0.024) were different between those two groups.
conclusionsThe authors demonstrated that normal [NAA] increase from PND8 to PND9 was impeded in sevoflurane-exposed rats when exposed at PND7; however, not impeded when exposed on PND15. Furthermore, the authors showed that noninvasive 1HMRS is sufficiently sensitive to detect subtle differences in developmental time trajectory of [NAA]. This is potentially clinically relevant because 1HMRS can be applied across species and may be useful in providing evidence of neurotoxicity in the human neonatal brain.
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