Neonatal sevoflurane exposure induces plasma biomarkers of inflammation in infant rhesus macaques.

Animal models and human studies suggest that general anesthesia exposure during infancy results in long-lasting neurocognitive impairments. Because millions of children each year undergo procedures that require anesthesia, it is important to investigate the mechanism of anesthesia induced neurotoxicity to ultimately develop ways to protect the vulnerable developing brain. Animal models have played a key role in this investigation and have shown that neonatal general anesthesia exposure results in neuronal apoptosis, long-term mitochondrial dysfunction, and astrogliosis. The current study involved a rhesus macaque model of repeated sevoflurane exposure that has been shown to produce cognitive deficits, behavioral changes, and mitochondrial damage. This study sought to investigate whether prolonged sevoflurane exposure induced inflammation as measured in peripheral blood samples. Results found that sevoflurane exposure resulted in changing levels of inflammatory markers in the periphery. Specifically, interleukin 6 (IL-6) was increased immediately following sevoflurane exposure, but not at 24-h post-exposure. Plasma samples collected 24-h after exposure revealed increased granulocyte macrophage colony-stimulating factor (GM-CSF), but decreased monocyte chemoattractant protein-4 (MCP-4) and interferon gamma-induced protein 10 (IP-10) levels. Changes in these markers have been linked to cognitive impairment, and together these data suggest that plasma levels of cytokines and chemokines are a good potential medium to investigate anesthesia-induced inflammation in clinical populations.