Dexmedetomidine-mediated neuroprotection against sevoflurane-induced neurotoxicity extends to several brain regions in neonatal rats

SEVO anaesthesia induced widespread apoptosis in infant rat brain. Co-administration of DEX (1 µg kg−1) provided significant protection, whereas DEX (5 µg kg−1 or higher) plus SEVO increased mortality. Our findings suggest that DEX could be an attractive therapeutic for future studies investigating its neuroprotective potential in a translational animal model.