Abstract
Delayed release of hemoglobin from the subarachnoid clot in the vicinity of conductive arteries leads to cerebral vasospasm after SAH. The mechanism of vasospasm however remains unclear. The one thousand times higher affinity of ferrous heme for nitric oxide, a potent vasodilator of cerebral vessels, than to oxygen, has led to the concept that hemoglobin scavenges nitric oxide and produces delayed cerebral vasospasm after SAH. For several years we have investigated the pathological mechanism(s) behind this event using in vivo experiments. We summarize experimental data and discuss the clinical value of the observations for the development of a new treatment for vasospasm after SAH.
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