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Acta Neurochir Suppl. 2011;110(Pt 1):105-9. doi: 10.1007/978-3-7091-0353-1_19.

Nitric oxide related pathophysiological changes following subarachnoid haemorrhage.

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Division of Neurosurgery, Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, and Department of Surgery, University of Toronto, Toronto, ON, Canada.


Subarachnoid hemorrhage (SAH) comprises only about 7% of all strokes worldwide but is associated with severe mortality and morbidity. SAH is associated with a number of secondary pathologies, such as: transient cerebral vasospasm, delayed ischemic neuronal deficit (DIND), cortical spreading depression, microcirculatory modifications, microthrombosis and ischemic complications. Available data demonstrate that there are complex interactions among these secondary complications, and NO plays an important role among the interactions. NO has been implicated to be a crucial molecule in eliminating vasospasm, facilitating neuroprotection, anti-microthrombosis, cerebral ischemic tolerance and promoting endothelial cell function. Therefore, therapeutic agent targeting a key component in the pathopyhysiology of SAH such as NO and its related enzymes would be favorable for future development of SAH drugs. Alternatively, because of the complex nature of the secondary complications after SAH, agents with multiple efficacies on these complications, or the combination of several agents such as NO donors, oxide radical scavengers and neuroprotectants might be more desirable.

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