Neurosurgery
-
Delayed cerebral vasospasm occurring after subarachnoid hemorrhage (SAH) is still responsible for a considerable percentage of the morbidity and mortality in patients with aneurysms. It has been suggested that the pathogenesis of delayed cerebral vasospasm is related to a number of pathological processes, including endothelial damage and smooth muscle cell contraction resulting from spasmogenic substances generated during lysis of subarachnoid blood clots, changes in vascular responsiveness, and inflammatory or immunological reactions of the vascular wall. It has been recognized that the endothelium plays an important role in the regulation of the cerebral vascular tone. In 1988, endothelin (ET)-1, a potent vasoconstrictor, was isolated from cultured porcine aortic endothelial cells. ⋯ The results of current clinical and experimental investigations support the hypothesis that ET-1 is a major cause of cerebral vasospasm after SAH. Other studies indicate that SAH causes complex changes in the ET system and increased ET-1 levels after SAH, which are not solely responsible for the development of vasospasm but may occur after cerebral ischemia. Further investigations are therefore needed to clarify these different hypotheses.