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心力衰竭中的炎症细胞因子和一氧化氮及迷走神经刺激的潜在调节作用。

Inflammatory cytokines and nitric oxide in heart failure and potential modulation by vagus nerve stimulation.

机构信息

Cardiac Electrophysiology, University of Iowa Hospitals, 200 Hawkins Drive, Room 4426a JCP, Iowa City, IA 52242, USA.

出版信息

Heart Fail Rev. 2011 Mar;16(2):137-45. doi: 10.1007/s10741-010-9184-4.

Abstract

In heart failure, an inflammatory response may occur. The relationship between inflammatory cytokines, NOS and heart failure progression remains uncertain. Parasympathetic activation can affect heart rate and AV conduction. In heart failure, a relationship between the vagus nerve and the inflammatory response has been proposed. Vagal nerve stimulation can modulate the inflammatory response and affect specific inflammatory mediators including nitric oxide that may be contributory to continued or progressive heart failure. Therefore, vagal nerve stimulation may have beneficial effects that are independent from heart rate or AV conduction in heart failure. Challenges remain regarding the relationship between specific inflammatory markers and heart failure and how to best modulate the cytokines and NOS in patients to achieve beneficial effects. Future studies need to evaluate whether modulating inflammatory cytokines and NOS via vagal nerve stimulation can improve cardiac performance and outcomes in patients with heart failure.

摘要

在心力衰竭中,可能会发生炎症反应。炎症细胞因子、NOS 与心力衰竭进展之间的关系尚不确定。副交感神经激活会影响心率和房室传导。在心力衰竭中,已提出迷走神经与炎症反应之间存在关系。迷走神经刺激可以调节炎症反应,并影响特定的炎症介质,包括可能有助于持续或进展性心力衰竭的一氧化氮。因此,迷走神经刺激可能具有独立于心率或房室传导的心力衰竭的有益作用。关于特定炎症标志物与心力衰竭之间的关系以及如何最佳调节细胞因子和 NOS 以达到有益效果,仍然存在挑战。未来的研究需要评估通过迷走神经刺激调节炎症细胞因子和 NOS 是否可以改善心力衰竭患者的心脏功能和结局。

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