To ensure adequate brain perfusion, multiple mechanisms tightly regulate cerebral blood flow (CBF) through myogenic, neurogenic, metabolic and endothelial factors in a process known as autoregulation [1]. Cerebral vasospasm is a disease of impaired autoregulation, resulting in reversible narrowing of blood vessels, often leading to stroke and poor patient outcomes [2-5]. It occurs in up to 50-90% of patients with aneurysmal subarachnoid hemorrhage (SAH) [6], and 60% of patients with traumatic brain injury [7], making it one of the leading causes of preventable morbidity in these patients [8-10]. Yet, there are limited durable treatment modalities for patients experiencing cerebral vasospasm; intra-arterial calcium channel blockers are moderately effective but short-acting, and balloon angioplasty has limited access to distal vessels with higher risks of vessel dissection and rupture.  Hence, targeted therapies to augment cerebral blood flow in disease states such as cerebral vasoconstriction are of immediate clinical importance. For my summer research project, I sought to investigate the feasibility of augmenting cerebral perfusion during cerebral vasospasm by pharmacologically blocking sympathetic outflow from the superior cervical ganglion.

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