Prevention And Treatment Of Vasospasm

Beyond rebleeding, vasospasm is one of the most feared consequences of aSAH because of its high rate of morbidity and mortality (14). Vasospasm occurs due to a complex cascade of parallel, yet interacting, biochemical pathways, likely including (i) endothelium-derived factors (including nitric oxide and oxygen free radicals), (ii) vascular smooth muscle-derived factors (e.g., calcium-channel activation and protein kinase C (PKC) activation), (iii) pro-inflammatory mediators (e.g., cysteines, histamine, and bradykinin), and (iv) stress-induced gene activation (e.g., heat shock proteins and heme oxygenase-1) (15). Ultimately, these pathways result in vascular constriction, vascular smooth muscle proliferation, reduced perfusion, and neuronal injury. Consequently, developing pharmacologic agents or interventions that target the underlying biochemical pathways that mediate vasospasm has become a major focus of aSAH research.

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