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.
- Sevoflurane diminishes neurogenesis and promotes ferroptosis in embryonic prefrontal cortex via inhibiting nuclear factor-erythroid 2-related factor 2 expression.
- Neonatal Anesthesia and Oxidative Stress.
- LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497-5p to upregulate NLRX1.
- Downregulation of HOTAIR reduces neuronal pyroptosis by targeting miR-455-3p/NLRP1 axis in propofol-treated neurons in vitro.
- MiRNA-384-5p targets GABRB1 to regulate ketamine-Induced Neurotoxicity in Neurons.