Dexmedetomidine (DEX), an α2-adrenergic agonist, has been widely used for anesthesia, pain control, and intensive care unit sedation. Besides sleep-like sedation, DEX has many other beneficial effects, such as anti-inflammation, antioxidation, and anticell death. Subarachnoid hemorrhage (SAH), a severe and potentially fatal form of stroke, is a complex disease that is divided into 2 phases: early brain injury and delayed cerebral ischemia. In each phase, several pathologic changes are involved, including disturbed intracranial homeostasis, metabolic failure, blood-brain barrier damage, vasospasm, microthrombosis, and cortical spreading depolarization. DEX has been shown to have an effect on these SAH-related pathologic processes. Research shows that DEX could serve as a protective therapy for patients with SAH due to its ability to maintain stable intracerebral homeostasis, balance coagulation-fibrinolysis, repair a damaged blood-brain barrier as well as prevent vasospasm and suppress cortical spreading depolarization by anti-inflammatory, antioxidative, antiapoptotic, and vasoconstriction-dilation effects. In this scoping review, we critically assess the existing data on the potential protective effect of DEX after SAH. So far, only 1 retrospective clinical trial assessing the effect of DEX on clinical outcomes after SAH has been performed. Hence, more trials are still needed as well as translational research bringing results from bench to bedside.
This review was supported in part by the National Institutes of Health (R21NS095166, R21NS110008), the American Heart Association (17GRNT33450010), and the Brain Aneurysm Foundation.
The authors have no conflicts of interest to disclose.
Address correspondence to: Sylvain Doré, PhD, FAHA, E-mail: sdore@ufl.edu.
Received March 27, 2020
Accepted August 5, 2020
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