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.
- Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8.
- Protective Effects of Xenon on Propofol-Induced Neurotoxicity in Human Neural Stem Cell-Derived Models.
- Neonatal exposure to propofol affects interneuron development in the piriform cortex and causes neurobehavioral deficits in adult mice.
- The expression of glucose transporters and mitochondrial division and fusion proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity.
- Inhibition of microRNA-375 ameliorated ketamine-induced neurotoxicity in human embryonic stem cell derived neurons.