Subarachnoid haemorrhage (SAH) following cerebral aneurysm rupture or trauma can 
result in the induction of secondary ischaemic brain damage via a decrease in 
microvascular perfusion, a disruption of the blood-brain barrier and consequent 
vasogenic oedema, and the delayed spasm of the major cerebral arteries (i.e. 
vasospasm). It is increasingly apparent that oxygen radical-induced, 
iron-catalyzed lipid peroxidation (LP) within the subarachnoid blood and 
vascular wall plays a key role in the occurrence of these secondary events. 
Tirilazad mesylate is a potent cytoprotective inhibitor of LP that works by a 
combination of radical scavenging and membrane stabilizing properties. It has 
been demonstrated to attenuate the acute and delayed vascular consequences of 
SAH and to protect the brain against ischaemic insults. Much of its action is 
mediated by an effect on the vascular endothelium, although it also appears to 
exert some direct neuroprotection and to inhibit LP in the subarachnoid blood. 
These actions of tirilazad in experimental SAH are reviewed.