School of Medicine, Universityof Electronic Science and Technology of China, Chengdu, China.
Department of Anesthesiology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, No. 32 West Second Section, First RingRoad, Chengdu, 610072, Sichuan, China.
BMC Anesthesiol. 2021 Jun 28;21(1):180. doi: 10.1186/s12871-021-01394-7.
Neuroprotection strategies after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR) remain key areas of basic and clinical research. This study was designed to investigate the neuroprotective effects of dexmedetomidine following resuscitation and potential mechanisms.
Anesthetized rats underwent 6-min asphyxia-based cardiac arrest and resuscitation, after which the experimental group received a single intravenous dose of dexmedetomidine (25 μg/kg). Neurological outcomes and ataxia were assessed after the return of spontaneous circulation. The serum levels and brain expression of inflammation markers was examined, and apoptotic cells were quantified by TUNEL staining.
Neuroprotection was enhanced by dexmedetomidine post-conditioning after the return of spontaneous circulation. This enhancement was characterized by the promotion of neurological function scores and coordination. In addition, dexmedetomidine post-conditioning attenuated the serum levels of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α at 2 h, as well as interleukin IL-1β at 2, 24, and 48 h. TUNEL staining showed that the number of apoptotic cells in the dexmedetomidine post-conditioning group was significantly reduced compared with the control group. Further western blot analysis indicated that dexmedetomidine markedly reduced the levels of caspase-3 and nuclear factor-kappa B (NF-κB) in the brain.
Dexmedetomidine post-conditioning had a neuroprotective effect against cerebral injury following asphyxia-induced cardiac arrest. The mechanism was associated with the downregulation of apoptosis and neuroinflammation.
心脏骤停/心肺复苏后神经保护策略仍然是基础和临床研究的重点领域。本研究旨在探讨右美托咪定复苏后对神经的保护作用及其潜在机制。
麻醉大鼠进行 6 分钟窒息性心脏骤停和复苏，复律后实验组给予单次静脉注射右美托咪定（25μg/kg）。自主循环恢复后评估神经功能预后和共济失调。检测血清炎症标志物水平和脑内表达，TUNEL 染色法定量检测凋亡细胞。
右美托咪定后处理增强了自主循环恢复后的神经保护作用。这种增强表现为促进神经功能评分和协调。此外，右美托咪定后处理可减轻复律后 2 小时促炎细胞因子肿瘤坏死因子（TNF）-α和复律后 2、24 和 48 小时白细胞介素（IL）-1β的血清水平。TUNEL 染色显示，右美托咪定后处理组的凋亡细胞数量明显少于对照组。进一步的 Western blot 分析表明，右美托咪定显著降低了大脑中半胱氨酸天冬氨酸蛋白酶-3 和核因子-κB（NF-κB）的水平。
右美托咪定后处理对窒息性心脏骤停后脑损伤具有神经保护作用。其机制与下调细胞凋亡和神经炎症有关。
