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本公众号每天分享一篇最新一期Anesthesia & Analgesia等SCI杂志的摘要翻译，敬请关注并提出宝贵意见 Dexmedetomidine-Mediated Prevention of Renal Ischemia-Reperfusion Injury Depends in Part on Cholinergic Anti-Inflammatory Mechanisms 背景与目的 器官缺血再灌注损伤常引起局部和全身炎症反应，进而加重器官损伤。这些炎症反应可由中枢神经系统调节，尤其是迷走神经和烟碱乙酰胆碱受体，它们是胆碱能抗炎途径的关键组成部分。激活胆碱能抗炎途径可抑制过度炎症反应，是预防肾脏等器官缺血再灌注损伤的潜在策略。 方 法 用α2肾上腺素能受体激动剂右旋美托咪定（Dex）治疗或不治疗双侧肾缺血/再灌注小鼠，测定其迷走神经活性、血浆乙酰胆碱、儿茶酚胺和炎症介质、肾组织损伤和细胞死亡。 结 果 Dex能显著增加颈迷走神经放电频率，平均达142Hz（P<0.001），并能保护肾脏大体形态和结构，减轻缺血再灌注后细胞凋亡。此外，与假手术组的乙酰胆碱释放量（84.7 pmol/L）相比，右美托咪定也显著增加到135.8 pmol/L（中位数）（P<0.001），并降低肾缺血/再灌注诱导的几种炎症介质的水平。通过迷走神经切断、脾切除术或联合应用α2肾上腺素能受体拮抗剂阿替帕唑，所有这些作用都被消除。 结 论 我们的研究表明，Dex除了对α2肾上腺素能受体有直接作用外，至少部分通过副交感神经系统激活的抗炎作用提供肾脏保护。 原始文献摘要 Jianbo Ma, MD,Qian Chen, MD, Juanjuan Li, MD,et al.Dexmedetomidine-Mediated Prevention of Renal Ischemia-Reperfusion Injury Depends in Part on Cholinergic Anti-Inflammatory Mechanisms.Anesth. Analg. 2020 Apr;130(4)；PMID：30346356 BACKGROUND: Organ ischemia-reperfusion injury often induces local and systemic inflammatory responses, which in turn worsen organ injury. These inflammatory responses can be regulated by the central nervous system, particularly by the vagal nerve and nicotinic acetylcholine receptors, which are the key components of cholinergic anti-inflammatory pathway. Activation of the cholinergic anti-inflammatory pathway can suppress excessive inflammatory responses and be a potential strategy for prevention of ischemia-reperfusion injury of organs including the kidney. METHODS: Vagal nerve activity, plasma acetylcholine, catecholamine and inflammatory mediators, renal tissue injury, and cell death were measured in mice with bilateral renal ischemia/reperfusion with or without treatment with dexmedetomidine (Dex), an α2-adrenergic receptor agonist. RESULTS: Dex significantly increased the discharge frequency of the cervical vagal nerve by up to 142 Hz (mean) (P < .001), and preserved kidney gross morphology and structure and attenuated cell apoptosis after ischemia-reperfusion. Furthermore, Dex also significantly increased acetylcholine release to 135.8 pmol/L (median) when compared to that (84.7 pmol/L) in the sham group (P < .001) and reduced the levels of several inflammatory mediators induced by renal ischemia/reperfusion. All the effects were abolished by vagotomy, splenectomy, or combinative administration of atipamezole, an α2-adrenergic receptor antagonist. CONCLUSIONS: Our findings suggest that Dex provides renoprotection, at least in part, through anti-inflammatory effects of the parasympathetic nervous system activation in addition to its direct actions on α2-adrenergic receptors. 麻醉学文献进展分享 贵州医科大学高鸿教授课题组 翻译：任文鑫 编辑：冯玉蓉 审校：王贵龙 |
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