Dexmedetomidine-induced neuroprotection: is it translational?

Wang Yunzhen, Han Ruquan, Zuo Zhiyi
2016 Translational Perioperative and Pain Medicine  
Dexmedetomidine is often used in anesthesia and critical care medicine practice to sedate patients. Its neuroprotective effects have been shown in various ischemic and hemorrhagic brain injury models of animals. Randomized clinical trials have indicated that dexmedetomidine can improve outcome of patients under intensive care. Clinical trials are needed to determine whether dexmedetomidine can provide neuroprotection against ischemic and hemorrhagic stroke. Dexmedetomidine has become a commonly
more » ... used drug in anesthesia and critical care medicine practice. The molar mass of dexmedetomidine is 200.28 g/mol with formula of C 13 H 16 N 2 . The generic name of dexmedetomidine is precedex or dexdor. It is a selective agonist of α 2 -adrenergic receptor with anxiolytic, sedative and analgesic effects. It provides sedation without inhibiting respiration. Patient can be cooperative or semi-arousal under the sedation with dexmedetomidine. Its main side-effects include bradycardia and hypotension, which can be treated pharmacologically. In this review, we will discuss the potential neuroprotective effects of dexmedetomidine. Evidences from animal models It has been reported that dexmedetomidine has neuroprotective effects in animals with various insults to the brain. Dexmedetomidine attenuates central sympathetic activity and decreases anesthetic requirements. Hoffman et al. deter-mined the effects of dexmedetomidine on neurological and histopathological outcome after incomplete cerebral ischemia in rats about 25 years ago [1]. The results show that dexmedetomidine given during brain ischemia improved neurological and histopathological outcome after incomplete ischemia in rats anesthetized with fentanyl and nitrous oxide. This effect was reversed by atipamezole, indicating that the effect is mediated by α 2 -adrenergic receptors. Improvement with dexmedetomidine was not mediated by changes in plasma glucose or other physiologic variables during ischemia. It was concluded that dexmedetomidine decreased ischemic brain injury after incomplete cerebral ischemia by decreasing sympathetic activity. In another study with using a model of focal cerebral ischemia caused by occluding the left internal carotid, anterior and middle cerebral arteries for 2 h [2], rabbits received dexmedetomidine or normal saline 10 min after the occlusion. A plasma level of dexmedetomidine was maintained at 4.0 ± 0.15 ng/ ml. The area of ischemic neuronal injury in the cortex was significantly decreased by about 47.6% in the group treated with dexmedetomidine. These results suggest that treatment with dexmedetomidine, at a dose to reduce the requirements of anesthetics by 50%, provides neuroprotection against focal cerebral ischemia. Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Ren et al. studied the effects of dexmedetomidine on seven-day old Sprague Dawley rats with left
doi:10.31480/2330-4871/044 fatcat:exuhwgufzfcvhkwiay3ze4mg4q