Molecular mechanisms for early brain injury after subarachnoid hemorrhage

Abstract

An increasing volume of experimental and clinical data indicates that early brain injury after initial bleeding largely contributes to unfavorable outcome and mortality after subarachnoid hemorrhage (SAH). Patients who recover from cerebral ischemia caused by intracranial pressure (ICP) raised over diastolic blood pressure suffer from severe injury to the brain tissues and cerebral microvasculature. This chapter aims to review: (1) pathophysiological factors and molecular agents acting on cerebral and vascular tissues after initial bleeding; (2) molecular responses to the early intracranial phenomena in SAH; (3) molecular signaling that contributes to the early development of pathological sequelae of SAH, including blood-brain barrier rupture, brain edema, and apoptosis; and (4) molecular mechanisms of cell death in the brain occurring early after SAH. © 2007 Springer-Verlag US.