Massa Christopher B, Allen Gilman B, Bates Jason H T
Univ. of Vermont, HSRF 228, 149 Beaumont Ave., Burlington, VT 05405-0075, USA.
J Appl Physiol (1985). 2008 Dec;105(6):1813-21. doi: 10.1152/japplphysiol.90806.2008. Epub 2008 Oct 23.
Lung recruitment and derecruitment contribute significantly to variations in the elastance of the respiratory system during mechanical ventilation. However, the decreases in elastance that occur with deep inflation are transient, especially in acute lung injury. Bates and Irvin (8) proposed a model of the lung that recreates time-varying changes in elastance as a result of progressive recruitment and derecruitment of lung units. The model is characterized by distributions of critical opening and closing pressures throughout the lung and by distributions of speeds with which the processes of opening and closing take place once the critical pressures have been achieved. In the present study, we adapted this model to represent a mechanically ventilated mouse. We fit the model to data collected in a previous study from control mice and mice in various stages of acid-induced acute lung injury (3). Excellent fits to the data were obtained when the normally distributed critical opening pressures were about 5 cmH(2)O above the closing pressures and when the hyperbolically distributed opening velocities were about an order of magnitude greater than the closing velocities. We also found that, compared with controls, the injured mice had markedly increased opening and closing pressures but no change in the velocities, suggesting that the key biophysical change wrought by acid injury is dysfunction of surface tension at the air-liquid interface. Our computational model of lung recruitment and derecruitment dynamics is thus capable of accurately mimicking data from mice with acute lung injury and may provide insight into the altered biophysics of the injured lung.
肺复张和肺萎陷在机械通气过程中对呼吸系统弹性的变化有显著影响。然而，深度充气时弹性的降低是短暂的，尤其是在急性肺损伤中。贝茨和欧文（8）提出了一个肺模型，该模型可重现由于肺单位的逐步复张和萎陷而导致的弹性随时间变化的情况。该模型的特点是整个肺中临界开放压和临界关闭压的分布，以及一旦达到临界压力后开放和关闭过程发生的速度分布。在本研究中，我们对该模型进行了调整，以代表机械通气的小鼠。我们将该模型与先前一项研究中从对照小鼠和处于酸诱导急性肺损伤各个阶段的小鼠收集的数据进行拟合。当正态分布的临界开放压比临界关闭压高约5 cmH₂O，且双曲线分布的开放速度比关闭速度大约一个数量级时，获得了与数据的良好拟合。我们还发现，与对照组相比，受伤小鼠的开放压和关闭压明显增加，但速度没有变化，这表明酸损伤引起的关键生物物理变化是气液界面表面张力的功能障碍。因此，我们的肺复张和萎陷动力学计算模型能够准确模拟急性肺损伤小鼠的数据，并可能为深入了解受伤肺的生物物理学改变提供帮助。
