Key points are not available for this paper at this time.
With the development of technology, more infants receive general anesthesia for surgery, other interventions, or clinical examination at an early stage after birth. However, whether general anesthetics can affect the function and structure of the developing infant brain remains an important, complex, and controversial issue. Sevoflurane is the most-used anesthetic in infants, but this drug is potentially neurotoxic. Short or single exposure to sevoflurane has a weak effect on cognitive function, while long or repeated exposure to general anesthetics may cause cognitive dysfunction. This review focuses on the mechanisms by which sevoflurane exposure during development may induce long-lasting undesirable effects on the brain. We review neural cell death, neural cell damage, impaired assembly and plasticity of neural circuits, tau phosphorylation, and neuroendocrine effects as important mechanisms for sevoflurane-induced developmental neurotoxicity. More advanced technologies and methods should be applied to determine the underlying mechanism(s) and guide prevention and treatment of sevoflurane-induced neurotoxicity. 1. We discuss the mechanisms underlying sevoflurane-induced developmental neurotoxicity from five perspectives: neural cell death, neural cell damage, assembly and plasticity of neural circuits, tau phosphorylation, and neuroendocrine effects. 2. Tau phosphorylation, IL-6, and mitochondrial dysfunction could interact with each other to cause a nerve damage loop. 3. miRNAs and lncRNAs are associated with sevoflurane-induced neurotoxicity.
Sun et al. (Fri,) studied this question.