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There is a growing body of evidence that suggests common complications inregional anesthesia, including transient neurological syndrome, are caused bythe neurotoxicity of local anesthetics (LAs). Ropivacaine is thought to be oneof the safest LAs, however, there have been several studies detailing possibleneurotoxic effects. At present, the exact molecular mechanism of ropivacaine-mediatedneurotoxicity is unknown. The present study was designed to explore the possiblemechanisms underlying the neurotoxicity of ropivacaine. The neurotoxic effectsof ropivacaine were assessed in spinal cord by TUNEL staining for apoptosis andin cultured PC12 cells by cell viability assays. Protein kinase B (Akt) activationwas evaluated by immunoblotting. Ropivacaine promoted apoptosis and caused celldeath in a treatment group compared with a sham-operated group. Furthermore, ropivacainesignificantly diminished Akt activation. There were significantly lower Akt levelsin cells exposed to ropivacaine compared with controls. The present study demonstratedropivacaine neurotoxicity in vivo and in vitro, mediated by the Akt signalingpathway. The neurotoxicity of apoptosis with concomitant cell death, mediatedby ropivacaine, may offer an explanation for its adverse effects (e.g., transientneurological syndrome).

In vivo and in vitro evidence of the neurotoxic effects of ropivacaine: The role of the Akt signaling pathway