ArticleMedical gas research2026
Anesthetic gas sevoflurane postconditioning alleviates cognitive impairment induced by hemorrhagic shock and resuscitation.
Article in Medical gas research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sevoflurane is a new type of halogen inhalation anesthetic gas with a rapid induction and emergence. It is widely used for general anesthesia. Previous studies have demonstrated that sevoflurane postconditioning alleviates cerebral ischemia-reperfusion injury and enhances the tolerance of the brain to ischemia and hypoxia. However, whether sevoflurane postconditioning can reduce cerebral ischemia-reperfusion injury caused by hemorrhagic shock and resuscitation and the underlying mechanism are unclear. The present study established cerebral ischemia-reperfusion injury models through an in vivo hemorrhagic shock and resuscitation method in C57BL/6 mice and an in vitro oxygen-glucose deprivation/reoxygenation method in HT22 cells. After hemorrhagic shock and resuscitation treatment, the mice developed significant spatial learning and memory impairments accompanied by aggravated cerebral infarction, whereas sevoflurane postconditioning significantly improved these effects. After in vitro oxygen-glucose deprivation/reoxygenation, the survival rate of HT22 cells was decreased, the apoptosis rate was increased, the expression of silent information regulatory factor 1 was decreased, and the expressions of hypoxia-inducible factor 1α, NOD-like receptor protein 3, gasdermin D, caspase-1, and interleukin-1β were increased. Sevoflurane postconditioning inhibited oxygen-glucose deprivation/reoxygenation-induced changes. Following silent information regulatory factor 1 knockdown by small interfering RNA, the cytoprotective effects of sevoflurane postconditioning were significantly attenuated. These findings suggest that the anesthetic gas sevoflurane postconditioning ameliorates hemorrhagic shock and resuscitation-induced cognitive impairment. This may be mediated by the silent information regulatory factor 1/hypoxia-inducible factor 1α/NOD-like receptor protein 3 pathway.
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