Mehmet Sorar1, Orhan Altay. 1. SBU Ankara Diskapi Yildirim Beyazit Training and Research Hospital, Department of Neurosurgery, Ankara, Turkey.
Abstract
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 groups in 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 brain edema (brain water content) were evaluated 24 h after SAH. Neuroglial cell death was examined by terminal deoxynucleotidyl transferase-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 neurobehavioral function, 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 the development of EBI after SAH, implying its use for anesthesia during acute aneurysm surgery or intervention.
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 groups in 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 brain edema (brain water content) were evaluated 24 h after SAH. Neuroglial cell death was examined by terminal deoxynucleotidyl transferase-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 neurobehavioral function, 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 the development of EBI after SAH, implying its use for anesthesia during acute aneurysm surgery or intervention.
Authors: Orhan Altay; Hidenori Suzuki; Bilge Nur Altay; Vahit Calisir; Jiping Tang; John H Zhang Journal: Neurosci Lett Date: 2020-06-06 Impact factor: 3.046