COVID-19患者神经损伤中的脑-肺相互作用

Tariq Janjua, L. Moscote-Salazar, William AF Perdomo
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引用次数: 0

摘要

新发现的冠状病毒(SARS-CoV-2)在感染人体后产生一系列病理变化。很大一部分感染COVID-19的危重患者将需要多种重症监护策略,以提供适当的支持,以增加有利进化的可能性。新型冠状病毒可通过呼吸道粘膜侵入,先后感染多种细胞类型,引起严重的炎症反应。脑神经损伤患者有与原发性和继发性病变相关的因素。肺损伤对脑的影响表现为缺氧、高碳酸血症、低碳酸血症、介质释放、神经毒性因子的存在和内皮细胞的激活。另一方面,脑损伤由于颅内压(ICP)升高而影响肺部。神经炎症现象的发展,交感神经系统的激活,以及通过下丘脑-垂体-肾上腺轴存在强烈的多巴胺能活动。研究表明,创伤性脑损伤后II型肺细胞在超微结构水平上受到损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Brain-lung Interaction in Neurotrauma in COVID-19 Patients
The recently described coronavirus (SARS-CoV-2) has produced a series of pathological changes after infection of the human body. A significant percentage of infected critically ill patients with COVID-19 will require multiple intensive care strategies to give appropriate support to increase the possibility of favorable evolution. The new coronavirus could invade using the respiratory mucosa and to infect various cell types successively creating a severe inflammatory response. Patients with cerebral neurotrauma have elements associated with the primary and secondary lesions. Lung injury impact brain with hypoxia, hypercapnia, hypocapnia, mediators release, presence of neurotoxic factors, and endothelial activation. On the other hand, brain injury impacts lungs due to increase in intracranial pressure (ICP). There is development of neuroinflammatory phenomena, the activation of sympathetic nervous system, and the presence of intense dopaminergic activity through the hypothalamic-pituitary-adrenal axis. Studies have demonstrated injury at the ultrastructural level in type II pneumocytes after traumatic brain injury.
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