Dexmedetomidine as an Analgesic Agent with Neuroprotective Properties: Experimental and Clinical Aspects

Dexmedetomidine (dexdor or precedex®) is considered as a sedative agent that is widely used as an adjuvant in general anesthesia and critical care medicine practice. There are many evidences indicating its neuroprotective properties especially in various ischemic and hemorrhagic brain injury models of animals. Clinical trials have shown that dexmedetomidine (DEX) can improve outcome of intensive care unit (ICU) patients. Also, DEX is appropriate for use as a non-opioid analgesic therapy whenever minimizing opioid-related side effects is necessary. The underlying mechanism of this drug is related to the activation of alpha-2 adrenergic receptors, causing inhibition of C-fibers and Aα-fibers in the peripheral nervous system. Alpha-2 adrenergic receptors centrally (in the locus coeruleus) prevent nociceptive neurotransmission through the spinal cord. Alpha-2 adrenergic receptors also presynaptically inhibit the release of norepinephrine, which disturbs depolarization and the pain signaling. In addition, recent studies indicate that in neurons, synthesis and release of acetylcholine and nitric oxide are affected by DEX that could be involved in the regulation of analgesic activity of the drug. Apart from the beneficial effects of the drug on the nervous system, there are potential adverse effects, such as hypotension and bradycardia, which can be treated pharmacologically and must be taken into consideration by clinicians.

کلیدواژه ها:

Dexmedetomidine ، Neuroprotection ، Pain ، Analgesia ، Non-opioid