The protective effects of sevoflurane on subarachnoid hemorrhage

Abstract

Sevoflurane has become an important volatile anesthetic in clinic and has been widely studied in recent years. Numerous studies have demonstrated the efficacy of sevoflurane in safeguarding against brain damage across various domains. For example, it has played a neuroprotective role in subarachnoid hemorrhage (SAH), traumatic brain injury, and ischemia/reperfusion injury. The ensuing critique will focus on the significance of sevoflurane in experimental SAH and shed light on the underlying mechanisms. The findings of the current investigation demonstrate that sevoflurane possesses neuroprotective capabilities and clarify that it effectively attenuates secondary damage resulting from SAH through anti-inflammatory and anti-apoptotic pathways. More specifically, sevoflurane is observed to mitigate arterial vasospasm, diminish microvascular thrombosis, and alleviate cerebral edema. In light of these discoveries, we maintain that sevoflurane exhibits significant promise in the management of SAH, and it merits additional investigation to facilitate its prompt clinical implementation. Therefore, a thorough understanding of the neuroprotective properties of sevoflurane is beneficial to exploring novel therapeutic solutions for SAH and providing clinicians with alternative treatment modalities.

Keywords: SAH; apoptosis; brain edema; inflammation; inhalation anesthetics; neuroprotection; sevoflurane; subarachnoid hemorrhage; vasospasm.

Figure 1:

The potential mechanism of sevoflurane against SAH. Note: Sevoflurane plays an important role in SAH via anti-inflammation, anti-apoptosis, reduce arterial spasm and microvascular thrombosis and other mechanisms. Bax: Bcl-2- associated X; BBB: blood-brain barrier; Bcl-2: B-cell lymphoma-2; BDNF: brain-derived neurotrophic factor; Caspase-3: cysteinyl aspartate specific proteinase-3; COX2: cyclooxygenase 2; HIF-1α: hypoxia-inducible factor-1α; IL-1β: interleukin-1β; IL-6: interleukin-6; SAH: subarachnoid hemorrhage; SphKI: sphingosine kinase 1; TNF-α: tumor necrosis factor-α; ZO-1: zonula occludens-1. Created with BioRender.com.