Inhibitory Effects of Dexmedetomidine and Propofol on Gastrointestinal Tract Motility Involving Impaired Enteric Glia Ca2+ Response in Mice
Inhibitory Effects of Dexmedetomidine and Propofol on Gastrointestinal Tract Motility Involving Impaired Enteric Glia Ca2+ Response in Mice
复制标题
右美托咪定和异丙酚对涉及肠胶质细胞 Ca2 反应受损的小鼠胃肠道运动的抑制作用
DOI：
10.1007/s11064-021-03280-7
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发表时间：
2021-03-03
影响因子：
4.4
通讯作者：
Wang, Qiang
中科院分区：
文献类型：
--
作者：
Li, Yansong;Wang, Yubo;Wang, Qiang
丙泊酚和右美托咪定是ICU常用的镇静剂，但其对胃肠道动力的影响尚未引起足够的重视。本研究旨在比较丙泊酚和右美托咪定在镇静水平下对胃肠道运动的影响，并探讨其可能的机制。雄性C57 BL/6小鼠（8-10周龄）随机分为对照组、丙泊酚组和右美托咪定组。腹腔注射异丙酚或右美托咪定后，通过镇静评分、生理参数和脑电图（EEG）证实了相当的镇静水平。评价了体内不同节段的GIT运动（胃排空、小肠传输、远端结肠珠排出、粪便重量和粪便颗粒数量、胃肠传输和全肠传输时间）和体外结肠移行运动复合体（CMMCs）模式。在丙泊酚或右美托咪定处理下，检测原代肠胶质细胞的Ca 2+反应。异丙酚50 mg/kg组与右美托咪定40 μg/kg组的生理参数和复合排列熵指数（CPEI）差异不大，达到了平行镇静水平。数据显示，丙泊酚和右美托咪定对GIT运动具有显著的抑制作用，而右美托咪定的抑制作用更强。此外，经镇静剂处理后，原代肠神经胶质细胞的钙反应幅度（ΔF/F0）明显降低，但右美托咪定的作用大于丙泊酚。这些结果表明，右美托咪定对镇静小鼠的GIT运动产生更强的抑制作用，这可能涉及肠胶质细胞中Ca 2+反应受损。因此，应谨慎使用右美托咪定，尤其是潜在GIT动力障碍患者。
Propofol and dexmedetomidine are popular used for sedation in ICU, however, inadequate attention has been paid to their effect on gastrointestinal tract (GIT) motility. Present study aimed to compare the effect of propofol and dexmedetomidine on GIT motility at parallel level of sedation and explore the possible mechanism. Male C57BL/6 mice (8-10 weeks) were randomly divided into control, propofol and dexmedetomidine group. After intraperitoneal injection of propofol or dexmedetomidine, comparable sedative level was confirmed by sedative score, physiological parameters and electroencephalogram (EEG). Different segments of GIT motility in vivo (gastric emptying, small intestine transit, distal colon bead expulsion, stool weight and number of fecal pellets, gastrointestinal transit and whole gut transit time) and colonic migrating motor complexes (CMMCs) pattern in vitro were evaluated. The Ca2+response of primary enteric glia was examined under the treatment of propofol or dexmedetomidine. There is little difference in physiological parameters and composite permutation entropy index (CPEI) between administration of 50 mg/kg propofol and 40 μg/kg dexmedetomidine, indicated that parallel level of sedation was reached. Data showed that propofol and dexmedetomidine had significantly inhibitory effect on GIT motility while dexmedetomidine was stronger. Also, the amplitude (ΔF/F0) of Ca2+response in primary enteric glia was attenuated after treated with the sedatives while the effect of dexmedetomidine was greater than propofol. These findings demonstrated that dexmedetomidine caused stronger inhibitory effects on GIT motility in sedative mice, which may involve impaired Ca2+response in enteric glia. Hence, dexmedetomidine should be carefully applied especially for potential GIT dysmotility patient.