Molecular mechanism of cerebral vasospasm induced by subarachnoid hemorrhage / 中国组织工程研究

ABSTRACT

OBJECTIVE:To investigate the molecular mechanism of cerebral vasospasm (CVS) from the perspectives of the basic molecular biology of cerebrovascular regulation, vascular cell proliferation, inflammatory reactions of vascular cells, and gene activation.DATA SOURCE By using the key words "subarachnoid hemorrhage","cerebral ischemia", "temporal", and "molecular biology", we retrieved the related articles between January 1998 and December 2004 in Medline,and the language was limited to English.STUDY SELECTION All articles related to our study purpose were setal subjects. Exclusion criteria Duplicated experiments. The rest of articles were searched for the full text.DATA EXTRACTION Totally 20 articles related to the molecular mechanism of CVS induced by subarachnoid hemorrhage (SAH) with or without randomized studies were selected, and 14 of them accorded with the inclusion criteria. The other 6 papers of duplicated study were excluded.oxygen radicals damage both cerebral endothelial and smooth muscle cells through the following possible mechanism increasing endothelial permeability, increasing intracellular calcium and inositol 1,4,5-triphosphate levlarize and show impaired relaxation after SAH. This may be due to a depletion of the energy metabolism causing a dysfunction of ion pumps or inhibition of potassium channels, which leads to membrane depolarization gene activation can relieve CVS.CONCLUSION: The patbogenesis of SAH-induced CVS may be related to a number of pathological processes, including endothelial damage, smooth muscle cell contraction resulting from dysfunction of ion pumps or PKC activation, vascular cell proliferation, inflammatory reaction of the vascular wall, and gene activation.