Background: Subarachnoid hemorrhage (SAH) is considered as a violent disease with high
rate of morbidity and mortality. Early brain injury (EBI) and delayed vasospasm are the two aspects of
this disease that are becoming research hotspots.
Objective: We aim to update the role of oxidative stress in the development of EBI and delayed cerebral
vasospasm after SAH.
Method: We reviewed early researches, and mainly discussed three aspects of contents: reactive oxygen
species (ROS) production, the role of oxidative stress in early brain injury and delayed vasospasm,
and clinical implications.
Results: There are several sources for the excessive generation of oxidants after SAH such as disrupted
mitochondrial respiration, upregulated enzymatic pathways, extracellular hemoglobin degradation and
depressed intrinsic antioxidant systems. Neuron apoptosis induced by ROS is one vital mechanism of
EBI. And extracellular hemoglobin degradation and nitric oxide synthases up-reputation are involved
in the pathogenesis of delayed cerebral vasospasm. Some antioxidants show significant neuroprotection
Conclusion: ROS production increases in SAH via mitochondria, hemoglobin or enzymatic pathway,
and it plays a vital important role in SAH. It seems that antioxidant therapy will be most effective as
one component in a treatment regime that attempts to address all the different pathways to EBI and
vasospasm following SAH.