Few if any issues received more attention in the field of pediatric perioperative care over the past decade than developmental anesthesia neurotoxicity. While the possibility of a plausible association between anesthesia and postoperative personality changes in children was first hypothesized more than 60 years ago,1 substantial concern on this subject has been ignited by seminal laboratory work, conducted 50 years later, where exposure of newborn rats to a mixture of anesthetics induced widespread apoptosis and persistent cognitive deficits in these animals.2 The initial mistrust and rejection generated by this publication in the anesthesia community have been rapidly transformed into an important public health concern after the robust confirmation of developmental anesthesia neurotoxicity in a variety of experimental models and, most importantly, with the availability of human epidemiological data suggesting an association between early life anesthesia exposure and subsequent neurocognitive disturbances.
- Overexpression of lncRNA Gm15621 alleviates apoptosis and inflammation response resulting from sevoflurane treatment through inhibiting miR-133a/Sox4.
- Role of autophagy in sevoflurane-induced neurotoxicity in neonatal rat hippocampal cells.
- The positive allosteric modulation of GABAA receptors mRNA in immature hippocampal rat neurons by midazolam affects receptor expression and induces apoptosis.
- Euxanthone Ameliorates Sevoflurane-Induced Neurotoxicity in Neonatal Mice.
- Toxicity mechanism of sevoflurane in neural stem cells of rats through DNA methylation.