Neurogenic pulmonary edema following acute stroke: The progress and perspective.
Neurogenic pulmonary edema following acute stroke: The progress and perspective.
复制标题
DOI：
10.1016/j.biopha.2020.110478
复制
发表时间：
2020-07
期刊：
影响因子：
--
通讯作者：
Jie Zhao;Nanxia Xuan;W. Cui;Bao-Ping Tian
中科院分区：
文献类型：
--
作者：
Jie Zhao;Nanxia Xuan;W. Cui;Bao-Ping Tian
急性脑卒中后神经源性肺水肿（NPE）是一种急性呼吸窘迫综合征（ARDS），具有起病急、肺间质液浸润明显、消退快等特点。NPE的病理过程以交感神经兴奋和儿茶酚胺的爆发性释放引起阻力血管收缩为中心。升高的全身阻力迫使流体进入肺循环，而肺循环超负荷诱导肺毛细血管压力升高，并进而损害肺泡毛细血管屏障。肺泡毛细血管屏障的损伤导致肺通气障碍、血液灌注障碍和氧合障碍。最终，NPE会导致中风后患者的预后进一步恶化。目前，我们缺乏特异性的生物学诊断指标和精心统一的诊断标准，这导致许多患者无法快速识别和/或准确诊断。没有药物对NPE有效。因此，了解如何通过识别危险因素来早期诊断NPE以及如何应用适当的治疗以避免预后恶化是重要的科学目标。本文将从急性脑卒中后NPE的病理生理机制、病因学、流行病学、临床诊断和早期预测、综合治疗策略和新药开发等方面阐述其研究进展。并提出了自己对NPE的思考和展望。
Neurogenic pulmonary edema (NPE) following acute stroke is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent pulmonary interstitial fluid infiltration and rapid resolution. The pathological process of NPE centers on sympathetic stimulation and fulminant release of catecholamines, which cause contraction of resistance vessels. Elevated systemic resistance forces fluid into pulmonary circulation, while pulmonary circulation overload induces pulmonary capillary pressure that elevates, and in turn damages the alveolar capillary barrier. Damage to the alveolar capillary barrier leads to pulmonary ventilation disorder, blood perfusion disorder and oxygenation disorder. Eventually, NPE will cause post-stroke patients’ prognosis to further deteriorate. At present, we lack specific biological diagnostic indicators and a meticulously unified diagnostic criterion, and this results in a situation in which many patients are not recognized quickly and/or diagnosed accurately. There are no drugs that are effective against NPE. Therefore, understanding how to diagnose NPE early by identifying the risk factors and how to apply appropriate treatment to avoid a deteriorating prognosis are important scientific goals. We will elaborate the progress of NPE after acute stroke in terms of its pathophysiological mechanisms, etiology, epidemiology, clinical diagnosis and early prediction, comprehensive treatment strategies, and novel drug development. We also propose our own thinking and prospects regarding NPE.