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A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
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Subarachnoid Hemorrhage and Sevoflurane.
1SBU Ankara Diskapi Yildirim Beyazit Training and Research Hospital, Department of Neurosurgery, Ankara, Turkey.
Turkish Neurosurgery
|March 23, 2019
Summary
Post-treatment sevoflurane administration protected against early brain injury in mice after subarachnoid hemorrhage. Specific concentrations and durations attenuated brain edema and neuronal cell death.
Area of Science:
- Neuroscience
- Anesthesiology
- Pharmacology
Background:
- Subarachnoid hemorrhage (SAH) frequently leads to early brain injury (EBI).
- Current treatments for SAH-induced EBI are limited.
- Sevoflurane's potential neuroprotective effects warrant investigation.
Purpose of the Study:
- To determine if post-treatment sevoflurane protects against EBI in a mouse model of SAH.
- To investigate the dose-dependent and time-dependent effects of sevoflurane on EBI.
- To explore the association between sevoflurane's neuroprotection and apoptosis inhibition.
Main Methods:
- SAH was induced in mice via endovascular perforation.
- Mice received varying concentrations (1.5%, 3%, 4.5%) and durations (30, 60, 90 min) of sevoflurane post-SAH.
- Neurobehavioral function, brain edema, and neuronal cell death (TUNEL staining) were assessed 24 hours post-SAH.
Main Results:
- Administration of 1.5% sevoflurane for 60 minutes improved neurobehavioral function and reduced brain edema.
- 3% sevoflurane for 30 or 60 minutes also significantly improved neurobehavioral function and reduced brain edema.
- Both effective sevoflurane regimens attenuated neuronal cell death in the basal cortex.
Conclusions:
- Post-treatment sevoflurane, specifically 1.5% for 60 min and 3% for 30-60 min, attenuates EBI after SAH in mice.
- These findings suggest sevoflurane may be beneficial during anesthesia for acute aneurysm surgery.
- Further research is needed to elucidate the precise mechanisms, including apoptosis inhibition.

