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肺血栓栓塞症中的肺表面活性物质改变。

Lung surfactant alterations in pulmonary thromboembolism.

机构信息

Department of Physiology, Jessenius Faculty of Medicine, Comenius University, Mala Hora 4, SK-03754 Martin, Slovakia.

出版信息

Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):38-41. doi: 10.1186/2047-783x-14-s4-38.

Abstract

Beside neonatal respiratory distress syndrome, secondary surfactant deficiency may occur in patients with mature lungs. Recent studies revealed quantitative and qualitative changes of lung surfactant in pulmonary thromboembolism (PTE) concerning the total phospholipids content in BAL fluid, alterations in surfactant phospholipids classes and a large-to-small aggregates ratio. Reduced expression of surfactant protein A (SP-A) mRNA and SP-A in lung tissue after pulmonary embolism was found. Serum levels of SP-A were significantly higher in patients with PTE than in other lung diseases, except COPD. Surfactant changes in PTE may result from damage of type II cells by hypoxia, leakage of plasma proteins into the airspaces and/or by reactive oxygen species. They can contribute to lung atelectasis and edema, and a further reduction in oxygen saturation as seen in clinical picture of PTE. Surfactant changes are reliable marker of lung injury that might become a prognostic indicator in patients with pulmonary thromboembolism.

摘要

除新生儿呼吸窘迫综合征外,成熟肺患者也可能发生继发性表面活性物质缺乏。最近的研究显示,肺血栓栓塞症(PTE)患者的肺表面活性物质存在定量和定性变化,与 BAL 液中的总磷脂含量、表面活性物质磷脂类别改变以及大-小聚集体比值有关。研究发现,肺栓塞后肺组织中表面活性物质蛋白 A(SP-A)mRNA 和 SP-A 的表达减少。PTE 患者的血清 SP-A 水平明显高于其他肺部疾病(除 COPD 外)。PTE 中的表面活性物质变化可能是由缺氧导致 II 型细胞损伤、血浆蛋白漏入肺泡腔和/或活性氧引起的。这些变化可能导致肺不张和水肿,并进一步降低 PTE 临床症状中的氧饱和度。表面活性物质变化是肺损伤的可靠标志物,可能成为肺血栓栓塞症患者的预后指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c0/3521350/98bbe5d30c0a/2047-783X-14-S4-38-1.jpg

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