Signaling mechanisms in cerebral vasospasm.
The elusive nature of events that sustain cerebral vasospasm after subarachnoid hemorrhage resulting from a ruptured aneurysm presents major challenges in designing effective therapies for this frequently devastating condition. Protracted cerebral artery constriction entails several dynamic components in intracellular signaling events initiated by endothelial factors, products of hemolysate, and numerous kinases, as well as increased intracellular Ca(2+). The rationale for potential treatment modalities and their efficacy are discussed in this brief review.
Nishizawa
Shigeru
S
Department of Neurosurgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Laher
Ismail
I
D017542:Aneurysm, Ruptured / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000503:physiopathology*; D003251:Constriction, Pathologic; D006801:Humans; D015398:Signal Transduction; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D013997:Time Factors; D020301:Vasospasm, Intracranial / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology