O'Brien William D, Kramer Jeffrey M, Waldrop Tony G, Frizzell Leon A, Miller Rita J, Blue James P, Zachary James F
Department of Electrical and Computer Engineering, University of Illinois, Urbana 61801, USA.
J Acoust Soc Am. 2002 Feb;111(2):1102-9. doi: 10.1121/1.1436068.
In a previous study [J. Acoust. Soc. Am. 108, 1290 (2000)] the acoustic impedance difference between intercostal tissue and lung was evaluated as a possible explanation for the enhanced lung damage with increased hydrostatic pressure, but the hydrostatic-pressure-dependent impedance difference alone could not explain the enhanced occurrence of hemorrhage. In that study, it was hypothesized that the animal's breathing pattern might be altered as a function of hydrostatic pressure, which in turn might affect the volume of air inspired and expired. The acoustic impedance difference between intercostal tissue and lung would be affected with altered lung inflation, thus altering the acoustic boundary conditions. In this study, 12 rats were exposed to 3 volumes of lung inflation (inflated: approximately tidal volume; half-deflated: half-tidal volume; deflated: lung volume at functional residual capacity), 6 rats at 8.6-MPa in situ peak rarefactional pressure (MI of 3.1) and 6 rats at 16-MPa in situ peak rarefactional pressure (MI of 5.8). Respiration was chemically inhibited and a ventilator was used to control lung volume and respiratory frequency. Superthreshold ultrasound exposures of the lungs were used (3.1-MHz, 1000-Hz PRF, 1.3-micros pulse duration, 10-s exposure duration) to produce lesions. Deflated lungs were more easily damaged than half-deflated lungs, and half-deflated lungs were more easily damaged than inflated lungs. In fact, there were no lesions observed in inflated lungs in any of the rats. The acoustic impedance difference between intercostal tissue and lung is much less for the deflated lung condition, suggesting that the extent of lung damage is related to the amount of acoustic energy that is propagated across the pleural surface boundary.
在之前的一项研究[《美国声学学会杂志》108, 1290 (2000)]中，评估了肋间组织与肺之间的声阻抗差异，以此作为随着静水压力增加肺损伤加重的一种可能解释，但仅静水压力依赖性阻抗差异无法解释出血发生率的增加。在该研究中，假设动物的呼吸模式可能会随静水压力而改变，这反过来可能会影响吸入和呼出的空气量。肋间组织与肺之间的声阻抗差异会随着肺膨胀的改变而受到影响，从而改变声学边界条件。在本研究中，12只大鼠暴露于3种肺膨胀量（充气：约潮气量；半放气：半潮气量；放气：功能残气量时的肺容积）下，6只大鼠处于8.6兆帕的原位峰值稀疏压力（声强为3.1），6只大鼠处于16兆帕的原位峰值稀疏压力（声强为5.8）。呼吸被化学抑制，并用呼吸机控制肺容积和呼吸频率。使用超阈值超声照射肺部（3.1兆赫、1000赫兹脉冲重复频率、1.3微秒脉冲持续时间、10秒照射持续时间）以产生损伤。放气的肺比半放气的肺更容易受损，半放气的肺比充气的肺更容易受损。事实上，在任何一只大鼠的充气肺中均未观察到损伤。放气肺状态下肋间组织与肺之间的声阻抗差异要小得多，这表明肺损伤的程度与穿过胸膜表面边界传播的声能量有关。
