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心力衰竭时肺气道阻力的显著增加:呼吸困难的一个潜在重要因素。

Profound Increase of Lung Airway Resistance in Heart Failure: a Potential Important Contributor for Dyspnea.

机构信息

Shanxi Provincial People's Hospital, Taiyuan, China.

Cardiovascular Division and Lillehei Heart Institute, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.

出版信息

J Cardiovasc Transl Res. 2019 Aug;12(4):271-279. doi: 10.1007/s12265-019-9864-y. Epub 2019 Jan 24.

DOI:10.1007/s12265-019-9864-y
PMID:30680546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7339933/
Abstract

Dyspnea is a major symptom of heart failure (HF). Here, we have studied the lung remodeling and airway resistance in HF mice. We demonstrated that aortic banding-induced HF caused a dramatic decrease of lung compliance and an increase of lung airway resistance. The decrease of lung compliance was correlated with the increased lung weight in a linear fashion (γ = 0.824). An HF-induced increase of lung airway resistance and a decrease of lung compliance were almost identical in anesthetized mice and in the isolated lungs from these mice. HF caused profound lung fibrosis in mice with increased lung weight. Moreover, HF patients of NYHA class III-IV showed increased lung density as revealed by high-resolution CT scanning. These data indicate that lung compliance and lung airway resistance may be useful in determining lung remodeling after HF, and lung structure changes may contribute to dyspnea in HF.

摘要

呼吸困难是心力衰竭(HF)的主要症状。在这里,我们研究了 HF 小鼠的肺部重塑和气道阻力。我们证明,主动脉缩窄诱导的 HF 导致肺顺应性显著下降和肺气道阻力增加。肺顺应性的下降与肺重量的线性增加呈正相关(γ=0.824)。HF 诱导的肺气道阻力增加和肺顺应性下降在麻醉小鼠和这些小鼠的离体肺中几乎相同。HF 导致小鼠肺部纤维化明显,肺重量增加。此外,NYHA 分级 III-IV 的 HF 患者通过高分辨率 CT 扫描显示肺密度增加。这些数据表明,肺顺应性和肺气道阻力可能有助于确定 HF 后的肺部重塑,并且肺结构变化可能导致 HF 中的呼吸困难。

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Basic Res Cardiol. 2017 May;112(3):25. doi: 10.1007/s00395-017-0615-4. Epub 2017 Mar 27.
2
T cell costimulation blockade blunts pressure overload-induced heart failure.T 细胞共刺激阻断削弱了压力超负荷诱导的心力衰竭。
Nat Commun. 2017 Mar 6;8:14680. doi: 10.1038/ncomms14680.
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CD28/B7 Deficiency Attenuates Systolic Overload-Induced Congestive Heart Failure, Myocardial and Pulmonary Inflammation, and Activated T Cell Accumulation in the Heart and Lungs.CD28/B7缺陷减轻收缩期负荷过重诱导的充血性心力衰竭、心肌和肺部炎症以及心脏和肺部活化T细胞的积聚。
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