Lambert Elisabeth, Schlaich Markus
Faculty of Health, Arts and Design, Iverson Health Innovations Research Centre, Swinburne University of Technology, Hawthorn, PO Box 218, Victoria 3122, Australia; Human Neuro-transmitters and Neurovascular Hypertension & Kidney Disease Laboratories, Baker IDI Heart & Diabetes Institute, Melbourne, Australia; Department of Physiology, Monash University, Clayton, Australia.
Human Neuro-transmitters and Neurovascular Hypertension & Kidney Disease Laboratories, Baker IDI Heart & Diabetes Institute, Melbourne, Australia; School of Medicine and Pharmacology, Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, University of Western Australia, Australia.
Auton Neurosci. 2017 May;204:105-111. doi: 10.1016/j.autneu.2017.01.002. Epub 2017 Jan 17.
Decreased blood flow supply to the kidneys known as renal ischemia/reperfusion is a common occurrence during various clinical and surgical settings. This remains highly concerning as it is a major cause of acute kidney injury (AKI). The kidneys have a rich supply of efferent and afferent sympathetic nerves playing a crucial physiological role in regulation of renal function. Studies in animal models of renal ischemia/reperfusion injury have indicated that very early during an ischemic event, the sympathetic nerves are activated and in concert with decreased nitric oxide availability, increased angiotensin II and several other molecules results in renal damage. Renal sympathetic inhibition or denervation seems to prevent or decrease some of the renal damage induced by ischemia/reperfusion injury but the evidence at present is based on animal studies and remains to be confirmed in the clinical setting. Remote ischemic preconditioning (IPC) has gained a lot of interest as a strategy to limit ischemia/reperfusion damage with some recent evidence suggesting that intact sympathetic nerves may be relevant in mediating protective effects. In this article, we review the experimental studies and emerging clinical studies that have investigated the role of sympathetic nerves following ischemia/reperfusion injury and studies exploring the role of sympathetic nerves in IPC and preventing tissue dysfunction induced by renal ischemia/reperfusion.
肾脏血流供应减少，即肾缺血/再灌注，在各种临床和手术情况下都很常见。这仍然是一个高度令人担忧的问题，因为它是急性肾损伤（AKI）的主要原因。肾脏有丰富的传出和传入交感神经供应，在肾功能调节中发挥着关键的生理作用。肾缺血/再灌注损伤动物模型的研究表明，在缺血事件的早期，交感神经就会被激活，并且与一氧化氮可用性降低、血管紧张素II增加以及其他几种分子共同作用导致肾损伤。肾交感神经抑制或去神经支配似乎可以预防或减少缺血/再灌注损伤引起的一些肾损伤，但目前的证据基于动物研究，仍有待在临床环境中得到证实。远程缺血预处理（IPC）作为一种限制缺血/再灌注损伤的策略引起了广泛关注，最近的一些证据表明完整的交感神经可能在介导保护作用方面具有相关性。在本文中，我们回顾了研究缺血/再灌注损伤后交感神经作用的实验研究和新兴临床研究，以及探索交感神经在IPC中的作用和预防肾缺血/再灌注诱导的组织功能障碍的研究。
