- 期刊
嗜中性白血球在急性呼吸窘迫症候群的角色：病理生理學上的重要性及治療趨勢
The Role of Neutrophils in Acute Respiratory Distress Syndrome: Review of Pathphysiological Significance and Current Treatments
摘要
急性呼吸窘迫症候群的起因多樣且複雜。病人主要特徵是肺部呈現急性兩側廣泛性浸潤及嚴重低血氧（PaO2/FiO2＜200mmHg）。病理切片可以發現肺組織中有大量嗜中性白血球的浸潤。嗜中性白血球主要是參與了急性呼吸窘迫症候群的病程進展，尤其在發炎反應滲出期，宿主支氣管肺泡灌洗液中，就會發現大量被活化且聚集在肺泡內；除此之外，也發現許多其相關的發炎介質：包括活性氧化物、白三烯素（發炎前驅分子）、基質金屬蛋白酶（破壞細胞膜）、血小板活化因子（趨化效應）等，並且會與細胞激素或化學趨化素交互作用，而破壞肺上皮及血管內皮細胞，加劇造成急性肺損傷。在動物研究及少數人體試驗已經證明：嗜中性白血球的活化、移行及發炎介質在急性呼吸窘迫症候群中扮演著很關鍵的角色。因此本文探討其與急性呼吸窘迫症候群的相關作用機轉，以期找到更有效的治療途徑。
並列摘要
The causes of acute respiratory distress syndrome (ARDS) are varied and complex. The main symptoms of patients with ARDS are acute bilateral diffuse infiltration in the lung and severe hypoxemia (PaO2/FiO2＜200mmHg). Neutrophils are generally involved in each process of ARDS. For example, neutrophils are activated and aggregated in the alveolar space during the exudative inflammatory phase. Many related inflammatory mediators are also found in the alveolar space, including reactive oxygen species, leukotrienes (inflammation precursor molecules), matrix metalloproteinases (which damage cell membranes), and platelet-activating substances (the chemotactic effect). Platelet-activating substances can also interact with cytokines or chemokines and lead to the destruction of lung epithelial and endothelial cells, which can aggravate acute lung injury. Recent studies on both animals and humans have demonstrated that neutrophils activation, migration, and inflammatory factors play key roles in the progression of ARDS. This paper describes the mechanism of neutrophils and progress in ARDS that we can find a more effective treatment strategy.
延伸閱讀
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