Department of Anatomy and Physiology, Kansas State University, Manhattan, KS, United States; Department of Clinical Sciences, Kansas State University, Manhattan, KS, United States.
Department of Anatomy and Physiology, Kansas State University, Manhattan, KS, United States; Department of Clinical Sciences, Kansas State University, Manhattan, KS, United States.
Auton Neurosci. 2014 Jul;183:111-5. doi: 10.1016/j.autneu.2014.02.009. Epub 2014 Mar 7.
Recent lines of inquiry indicate that sedatives can influence the immune system, leading to the concept of sedative-induced immunomodulation. It has been hypothesized that sedatives may alter immune responses by modulating the sympathetic nervous system, however, little information is known regarding the effects of sedatives on regulation of splenic sympathetic nerve discharge (SND), a significant omission based on the functional role that changes in splenic SND exert on splenic cytokine gene expression. The present investigation determined the effect of systemic Dexmedetomidine (Dex) administration on the level of directly-recorded splenic SND and tested the hypothesis that the intravenous administration of Dex would inhibit splenic SND in anesthetized rats. The present results demonstrate for the first time that intravenous Dex administration significantly reduces splenic sympathetic nerve outflow in baroreceptor-intact and sinoaortic-denervated rats, indicating that Dex administration alters the central regulation of splenic SND. The present results provide new information regarding the effect of a centrally-acting alpha2-adrenergic agonist on the level of sympathetic nerve outflow to a secondary lymphoid organ that plays a critical role in peripheral immune responses.
最近的研究表明，镇静剂可以影响免疫系统，从而产生镇静剂诱导免疫调节的概念。有人假设，镇静剂可能通过调节交感神经系统来改变免疫反应，但是，关于镇静剂对脾脏交感神经放电（SND）调节的影响知之甚少，鉴于 SND 的变化对脾脏细胞因子基因表达的功能作用，这是一个重大遗漏。本研究旨在确定全身给予右美托咪定（Dex）对直接记录的脾脏 SND 水平的影响，并验证静脉给予 Dex 会抑制麻醉大鼠脾脏 SND 的假设。目前的结果首次表明，静脉内给予 Dex 可显著降低完整和去窦弓神经大鼠的脾脏交感神经传出，表明 Dex 给药改变了脾脏 SND 的中枢调节。目前的结果提供了有关中枢作用的α2-肾上腺素能激动剂对发挥外周免疫反应关键作用的次级淋巴器官传出交感神经水平的影响的新信息。
