Advances in experimental subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) remains to be a devastating disease with high mortality and morbidity. Two major areas are becoming the focus of the research interest of SAH: these are cerebral vasospasm (CVS) and early brain injury (EBI). This mini review will provide a broad summary of the major advances in experimental SAH during the last 3 years. Treatments interfering with nitric oxide (NO)- or endothelin-pathways continue to show antispasmotic effects in experimental SAH. HIF 1 may play both a detrimental and beneficial role in the setting of SAH, depending on its activation stage. Inflammation and oxidative stress contribute to the pathophysiology of both CVS and EBI. Apoptosis, a major component of EBI after SAH, also underlie the etiology of CVS. Since we recognize now that CVS and EBI are the two major contributors to the significant mortality and morbidity associated with SAH, ongoing research will continue to elucidate the underlying pathophysiological pathways and treatment strategies targeting both CVS and EBI may be more successful and improve outcome of patients with SAH.