Dixon Dani-Louise, De Pasquale Carmine G, De Smet Hilde R, Klebe Sonja, Orgeig Sandra, Bersten Andrew D
Intensive and Critical Care Unit, Flinders Medical Centre, Bedford Park, Adelaide, South Australia 5042, Australia.
Am J Respir Crit Care Med. 2009 Jul 15;180(2):181-7. doi: 10.1164/rccm.200809-1506OC. Epub 2009 Apr 16.
Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung that reduce alveolar fluid filtration and protect against pulmonary microvascular rupture.
To determine whether these compensatory responses may have maladaptive effects on lung function.
Six weeks after myocardial infarction (chronic heart failure model) rat lung composition, both gross and histologic; air and saline mechanics; surfactant production; and immunological mediators were examined.
An increase in dry lung weight, due to increased insoluble protein, lipid and cellular infiltrate, without pulmonary edema was found. Despite this, both forced impedance and air pressure-volume mechanics were normal. However, there was increased tissue stiffness in the absence of surface tension (saline pressure-volume curve) with a concurrent increase in both surfactant content and alveolar type II cell numbers, suggesting a novel homeostatic phenomenon.
These studies suggest a compensatory reduction in pulmonary surface tension that attenuates the effect of lung parenchymal remodeling on lung mechanics, hence work of breathing.
慢性心力衰竭时肺微血管压力的持续升高会导致肺部出现代偿性变化，从而减少肺泡液体滤过并防止肺微血管破裂。
确定这些代偿反应是否可能对肺功能产生不良影响。
在心肌梗死（慢性心力衰竭模型）六周后，对大鼠肺的组成（大体和组织学）、空气和盐水力学、表面活性剂产生以及免疫介质进行检查。
发现由于不溶性蛋白质、脂质和细胞浸润增加，肺干重增加，但无肺水肿。尽管如此，强迫阻抗和气压 - 容积力学均正常。然而，在没有表面张力的情况下（盐水压力 - 容积曲线）组织硬度增加，同时表面活性剂含量和II型肺泡细胞数量均增加，提示一种新的稳态现象。
这些研究表明肺表面张力的代偿性降低减弱了肺实质重塑对肺力学的影响，进而减弱了呼吸功。
