title: Molecular keys to the problems of cerebral vasospasm.
abstract: The mechanisms responsible for subarachnoid hemorrhage (SAH)-induced vasospasm are under intense investigation but remain incompletely understood. A consequence of SAH-induced vasospasm, cerebral infarction, produces a nonrecoverable ischemic tissue core surrounded by a potentially amenable penumbra. However, successful treatment has been inconsistent. In this review, we summarize the basic molecular biology of cerebrovascular regulation, describe recent developments in molecular biology to elucidate the mechanisms of SAH-induced vasospasm, and discuss the potential contribution of cerebral microcirculation regulation to the control of ischemia. Our understanding of the pathogenesis of SAH-induced vasospasm remains a major scientific challenge; however, molecular biological techniques are beginning to uncover the intracellular mechanisms involved in vascular regulation and its failure. Recent findings of microvascular regulatory mechanisms and their failure after SAH suggest a role in the development and size of the ischemia. Progress is being made in identifying the various components in the blood that cause SAH-induced vasospasm. Thus, our evolving understanding of the underlying molecular mechanism may provide the basis for improved treatment after SAH-induced vasospasm, especially at the level of the microcirculation.
authors.affiliation: Department of Neurological Surgery, Washington University, St. Louis, Missouri 63110, USA.
authors.forename: H H
authors.initials: HH
authors.lastname: Dietrich
authors.forename: R G
authors.initials: RG
authors.lastname: Dacey
mesh_terms: D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology; D015316:Genetic Therapy; D006801:Humans; D008833:Microcirculation / Q000502:physiology; D008967:Molecular Biology / Q000379:methods*; D013345:Subarachnoid Hemorrhage / Q000150:complications; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy