Isoflurane versus sevoflurane for early brain injury and expression of sphingosine kinase 1 after experimental subarachnoid hemorrhage.

• 2% Isoflurane and 3% sevoflurane are neuroprotective equally. • Isoflurane and sevoflurane are effective against early brain injury after SAH. • Isoflurane and sevoflurane suppress post-SAH apoptosis and brain inflammation. • Effect of isoflurane and sevoflurane is mediated by sphingosine-related pathway. • Isoflurane and sevoflurane are good candidates for neuroanesthesia after SAH. The first step to treat aneurysmal subarachnoid hemorrhage (SAH) is aneurysmal obliteration under general anesthesia but not treat the SAH itself and the secondary effects. However, the identification of anesthetics with properties that help to attenuate post-SAH brain injury can be useful for improving outcomes of SAH patients. We examined whether 2% isoflurane and 3% sevoflurane posttreatment are protective against early brain injury (EBI) after SAH. This study used 87 8-week-old male CD-1 mice. We induced SAH by endovascular perforation in mice. Animals were randomly divided into 4 groups: sham-operated (n = 16), SAH + vehicle-medical air (n = 26), SAH + 2% isoflurane (n = 22), and SAH + 3% sevoflurane (n = 23). Neurobehavioral function, brain water content and Western blotting were evaluated at 24 h. The expression of sphingosine kinase (SphK), cleaved caspase-3 and cyclooxygenase-2 (COX2) was determined by Western blotting. Cell death was examined by terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end-labeling staining. Both 2% isoflurane and 3% sevoflurane significantly improved neurobehavioral function, and brain edema at 24 h after SAH and attenuated cell death, associated with an increase in SphK1, a decrease in cleaved caspase-3 and COX2. The neuroprotective effects were similar between 2% isoflurane and 3% sevoflurane. These findings suggest that both 2% isoflurane and 3% sevoflurane significantly inhibited EBI by suppressing post-SAH apoptosis and brain inflammation possibly via the SphK1-related pathway. [ABSTRACT FROM AUTHOR]