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519896 
Journal Article 
Mechanisms of acute brain injury after subarachnoid hemorrhage 
Sehba, FA; Bederson, JB 
2006 
1 
Neurological Research
ISSN: 0161-6412
EISSN: 1743-1328 
28 
4 
381-398 
English 
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. 
ischemia; cerebral blood flow; microvasculature; neuronal injury; mechanisms; cerebral-blood-flow; nitric-oxide synthase; canine basilar artery; no-reflow phenomenon; smooth-muscle-cells; spontaneously hypertensive; rats; ischemic neurological deficits; intimal platelet accumulation; barrier permeability changes; high-dose methylprednisolone