Files
Abstract
Subarachnoid Hemorrhage (SAH) is a devastating form of stroke caused by rupture of a large cerebral artery. This catastrophic event is associated with high mortality and long term neurological disability. SAH is also associated with other complications, which are severe and common. The complications are biphasic in nature, with some appearing very early after ictus such as acute hydrocephalus and cerebral edema, while others manifest days later; for example, delayed cerebral ischemia (DCI). The mechanisms underlying these complications are poorly understood but growing evidence suggests that dysfunction of the cerebral microvasculature plays a significant role in their development. The work in this thesis will first seek to characterize one of the earliest causes of impaired microvascular perfusion after SAH related to impaired CSF flow. Second, this work will study changes in the epoxyeicosanoid pathway in humans after SAH and then test its role as a protective mechanism in both early and delayed microvascular dysfunction.