Department of Neurosurgery, Second Affiliated Hospital of Shantou University Medical College, Shantou, China.
Department of Physiology of Visceral Function and Body Fluid, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Eur J Neurosci. 2022 Mar;55(6):1645-1657. doi: 10.1111/ejn.15648. Epub 2022 Mar 20.
Neurogenic pulmonary oedema (NPE) is a life-threatening complication that develops rapidly and dramatically after an injury to the central nervous system (CNS). The autonomic system imbalance produced by severe brain damage may play an important role in the development of NPE. Activation of the sympathetic nervous system and inhibition of the vagus nerve system are essential prerequisites for autonomic system imbalance. The more severe the damage, the more pronounced the phenomenon. Sympathetic hyperactivity is associated with increased release of catecholamines from peripheral sympathetic nerve endings, which can cause dramatic changes in haemodynamics and cause pulmonary oedema. On the other hand, the abnormal inflammatory response caused by vagus nerve inhibition may also play an important role in the pathogenesis of NPE. The perspective of autonomic system imbalance seems to perfectly integrate the existing pathogenesis of NPE and can explain the entire development progression of NPE.
神经源性肺水肿(NPE)是一种危及生命的并发症,在中枢神经系统(CNS)损伤后迅速而显著地发展。严重脑损伤引起的自主神经系统失衡可能在 NPE 的发展中起重要作用。交感神经系统的激活和迷走神经抑制是自主神经系统失衡的必要前提。损伤越严重,现象越明显。交感神经活性增加与外周交感神经末梢儿茶酚胺的释放增加有关,可引起血液动力学的剧烈变化,并导致肺水肿。另一方面,迷走神经抑制引起的异常炎症反应也可能在 NPE 的发病机制中起重要作用。自主神经系统失衡的观点似乎完美地整合了现有的 NPE 发病机制,并能解释 NPE 的整个发展过程。