右美托咪定减少了向疑核中的心迷走神经元的抑制性神经传递，但不影响兴奋性神经传递。
Dexmedetomidine decreases inhibitory but not excitatory neurotransmission to cardiac vagal neurons in the nucleus ambiguus.
作者信息
Sharp Douglas B, Wang Xin, Mendelowitz David
机构信息
Department of Anesthesiology and Critical Care Medicine, The George Washington University, USA.
Department of Pharmacology and Physiology, The George Washington University, 2300 Eye St. NW, Washington, DC 20037, USA.
出版信息
Brain Res. 2014 Jul 29;1574:1-5. doi: 10.1016/j.brainres.2014.06.010. Epub 2014 Jun 13.
Abstract
Dexmedetomidine, an α2 adrenergic agonist, is a useful sedative but can also cause significant bradycardia. This decrease in heart rate may be due to decreased central sympathetic output as well as increased parasympathetic output from brainstem cardiac vagal neurons. In this study, using whole cell voltage clamp methodology, the actions of dexmedetomidine on excitatory glutamatergic and inhibitory GABAergic and glycinergic neurotransmission to parasympathetic cardiac vagal neurons in the rat nucleus ambiguus was determined. The results indicate that dexmedetomidine decreases both GABAergic and glycinergic inhibitory input to cardiac vagal neurons, with no significant effect on excitatory input. These results provide a mechanism for dexmedetomidine induced bradycardia and has implications for the management of this potentially harmful side effect.
摘要
右美托咪定是一种α2肾上腺素能激动剂，是一种有效的镇静剂，但也可引起显著的心动过缓。心率下降可能是由于中枢交感神经输出减少以及脑干心脏迷走神经神经元的副交感神经输出增加所致。在本研究中，使用全细胞膜片钳技术，确定了右美托咪定对大鼠疑核中副交感心脏迷走神经神经元的兴奋性谷氨酸能、抑制性γ-氨基丁酸能和甘氨酸能神经传递的作用。结果表明，右美托咪定减少了对心脏迷走神经神经元的γ-氨基丁酸能和甘氨酸能抑制性输入，对兴奋性输入无显著影响。这些结果为右美托咪定诱导的心动过缓提供了一种机制，并对这种潜在有害副作用的管理具有重要意义。
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