It has become increasingly evident that the pathophysiology of cerebral vas
ospasm following subarachnoid hemorrhage (SAH) which described the ischemic
consequences of cerebral arterial constriction is complex and multifactori
al In an attempt to study cerebral vasospasm, numerous investigators have u
sed experimental animal models that resemble cerebral vasospasm in humans.
No ideal model for SAH has been found as yet, and hence the quest for such
a model continues. We developed an endoscopic technique that permits a dire
ct vision of internal carotid artery and puncturing the artery to provoke S
AH. This model will closely reflect the clinical setting of an aneurysm rup
ture. The onset of SAH was characterized by a sudden decrease of cerebral b
lood flow (CBF) and cerebral blood volume (CBV) by at least 40% in the firs
t 20 min. Following this initial drop, there was an increase in the CBF and
the CBV, however, they remained significantly below the base line values,
at the end of 1h. This study describes a new model of SAH in rat that simul
ates the clinical phenomenon of ruptured intracranial aneurysm that also pr
oduces cerebral vasospasm.