Nitric Oxide Related Pathophysiological Changes Following Subarachnoid Haemorrhage
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 complix 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.
KeywordseNOS Microthrombosis Nitric oxide (NO) Oxidative stress Subarachnoid hemorrhage (SAH)
This research is supported by funding from Physician Service Incorporated Ontario, Brain Aneurism Foundation to Dr. R Loch Macdonald.
Conflict of interest statement Dr. R. Loch Macdonald is a consultant for Actelion Pharmaceuticals. He is chief scientific officer of Edge Therapeutics.
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