Subarachnoid Hemorrhage and Sevoflurane

Özet

AIM: To examine whether post-treatment sevoflurane is protective against early brain injury (EBI) after subarachnoid hemorrhage(SAH) and how this neuroprotective effect occurs at different concentrations and durations of administration in mice. Furthermore,we tested whether the neuroprotective effect of post-treatment sevoflurane is associated with inhibition of apoptosis.MATERIAL and METHODS: SAH was induced in mice by endovascular perforation. Animals were randomly assigned to five groupsin each study. Study 1, sham-operated; SAH+vehicle-air; and SAH+1.5% sevoflurane for 30, 60, and 90 min. Study 2, SAH+3%sevoflurane for 30, 60, and 90 min. Study 3, SAH+4.5% sevoflurane for 30, 60, and 90 min. Neurobehavioral function and brainedema (brain water content) were evaluated 24 h after SAH. Neuroglial cell death was examined by terminal deoxynucleotidyltransferase-mediated uridine 5′-triphosphate-biotin nick end-labeling (TUNEL) staining.RESULTS:Administration of 1.5% sevoflurane for 60 min and 3% sevoflurane for 30 and 60 min significantly improved neurobehavioralfunction, brain edema, and attenuated neuronal cell death in the basal cortex at 24 h after SAH.CONCLUSION: Administration of 1.5% sevoflurane for 60 min and 3% for 30 and 60 min sevoflurane application attenuated thedevelopment of EBI after SAH, implying its use for anesthesia during acute aneurysm surgery or intervention.