Abstract
Dexmedetomidine, selective α2-adrenergic agonist dexmedetomidine, has been widely used clinically for sedation and anesthesia. The role of dexmedetomidine has been an interesting topic of neonatological and anesthetic research since a series of advantages of dexmedetomidine, such as enhancing recovery from surgery, reducing opioid prescription, decreasing sympathetic tone, inhibiting inflammatory reactions, and protecting organs, were reported. Particularly, an increasing number of animal studies have demonstrated that dexmedetomidine ameliorates the neurological outcomes associated with various brain and spinal cord injuries. In addition, a growing number of clinical trials have reported the efficacy of dexmedetomidine for decreasing the rates of postoperative neurological dysfunction, such as delirium and stroke, which strongly highlights the possibility of dexmedetomidine functioning as a neuroprotective agent for future clinical use. Mechanism studies have linked dexmedetomidine’s neuroprotective properties with its modulation of neuroinflammation, apoptosis, oxidative stress, and synaptic plasticity via the α2-adrenergic receptor, dependently or independently. By reviewing recent advances and preclinical and clinical evidence on the neuroprotective effects of dexmedetomidine, we hope to provide a complete understanding of the above mechanism and provide insights into the potential efficacy of this agent in clinical use for patients.
Highlights
Car accidents and falls are the main causes of nerve and brain injuries that can lead to permanent damage and dysfunction of a limb [1]
This work demonstrates the role of DEXM as a neuroprotective agent, which has been tested in various experimental models
It has been corroborated from the literature survey that DEXM abolishes its neuroprotective effects through the upregulation of α2 adrenoreceptor
Summary
Car accidents and falls are the main causes of nerve and brain injuries that can lead to permanent damage and dysfunction of a limb [1]. It attenuates delirium, improves postoperative cognitive dysfunction, and acts as a sympatholytic agent [11,12,13] It caught the attention of researchers and clinicians due to its cardioprotective [14], renoprotective [15], pulmonoprotective [16], and neuroprotective effects [17]. There has been very limited research regarding DEXM as a neuroprotective agent against neuronal injury and only a few review articles have been reported. To the authors’ best knowledge, there is not a single review article on the neuroprotective effect of DEXM against neuronal injury. DEXM is FDA approved IV drug that extensively undergoes a first-pass effect with a bioavailability of 16% [18] It shows a better intranasal sedative and anxiolytic effect in comparison to clonidine [19]. The average half-life of DEXM in a healthy individual is 2.1–3.1 h, while in ICU it is 2.2–3.7 h
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