title: Mechanisms of acute brain injury after subarachnoid hemorrhage.
abstract: Brain injury after subarachnoid hemorrhage (SAH) is a biphasic event with an acute ischemic insult at the time of the initial bleed and secondary events such as cerebral vasospasm 3 to 7 days later. Although much has been learned about the delayed effects of SAH, less is known about the mechanisms of acute SAH-induced injury. Distribution of blood in the subarachnoid space, elevation of intracranial pressure, reduced cerebral perfusion and cerebral blood flow (CBF) initiates the acute injury cascade. Together they lead to direct microvascular injury, plugging of vessels and release of vasoactive substances by platelet aggregates, alterations in the nitric oxide (NO)/nitric oxide synthase (NOS) pathways and lipid peroxidation. This review will summarize some of these mechanisms that contribute to acute cerebral injury after SAH.
authors.affiliation: Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY 10029-6574, USA. fatima.sehba@mssm.edu
authors.forename: Fatima A
authors.initials: FA
authors.lastname: Sehba
authors.forename: Joshua B
authors.initials: JB
authors.lastname: Bederson
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000209:etiology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D015227:Lipid Peroxidation / Q000502:physiology; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010974:Platelet Aggregation / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000503:physiopathology
chemical_list: D009569:Nitric Oxide; D019001:Nitric Oxide Synthase