Wu You, Nguyen Tam L, Perlman Carrie E
Biomedical Engineering, Chemistry and Biological Sciences, Stevens Institute of Technology, Hoboken, New Jersey.
Biomedical Engineering, Chemistry and Biological Sciences, Stevens Institute of Technology, Hoboken, New Jersey
J Appl Physiol (1985). 2017 Apr 1;122(4):739-751. doi: 10.1152/japplphysiol.00526.2016. Epub 2016 Dec 15.
Edematous lungs contain regions with heterogeneous alveolar flooding. Liquid is trapped in flooded alveoli by a pressure barrier-higher liquid pressure at the border than in the center of flooded alveoli-that is proportional to surface tension, Stress is concentrated between aerated and flooded alveoli, to a degree proportional to Mechanical ventilation, by cyclically increasing , injuriously exacerbates stress concentrations. Overcoming the pressure barrier to redistribute liquid more homogeneously between alveoli should reduce stress concentration prevalence and ventilation injury. In isolated rat lungs, we test whether accelerated deflation can overcome the pressure barrier and catapult liquid out of flooded alveoli. We generate a local edema model with normal by microinfusing liquid into surface alveoli. We generate a global edema model with high by establishing hydrostatic edema, which does not alter , and then gently ventilating the edematous lungs, which increases at 15 cmHO transpulmonary pressure by 52%. Thus ventilation of globally edematous lungs increases , which should increase stress concentrations and, with positive feedback, cause escalating ventilation injury. In the local model, when the pressure barrier is moderate, accelerated deflation causes liquid to escape from flooded alveoli and redistribute more equitably. Flooding heterogeneity tends to decrease. In the global model, accelerated deflation causes liquid escape, but-because of elevated -the liquid jumps to nearby, aerated alveoli. Flooding heterogeneity is unaltered. In pulmonary edema with normal , early ventilation with accelerated deflation might reduce the positive feedback mechanism through which ventilation injury increases over time. We introduce, in the isolated rat lung, a new model of pulmonary edema with elevated surface tension. We first generate hydrostatic edema and then ventilate gently to increase surface tension. We investigate the mechanical mechanisms through which ) ventilation injures edematous lungs and ) ventilation with accelerated deflation might lessen ventilation injury.
水肿肺包含肺泡充盈情况各异的区域。液体被一种压力屏障困在充盈的肺泡中,该压力屏障在肺泡边界处的液体压力高于其中心处,且与表面张力成正比。应力集中在通气肺泡和充盈肺泡之间,其程度与机械通气成正比,通过周期性增加,会有害地加剧应力集中。克服压力屏障以使液体在肺泡间更均匀地重新分布,应能降低应力集中的发生率和通气损伤。在离体大鼠肺中,我们测试加速放气是否能克服压力屏障并将液体从充盈的肺泡中弹射出来。我们通过向表面肺泡微量注入液体来建立具有正常表面张力的局部水肿模型。我们通过建立静水压性水肿来生成具有高表面张力的整体水肿模型,该模型不会改变表面张力,然后轻柔地对水肿肺进行通气,这会使跨肺压为15 cmH₂O时的表面张力增加52%。因此,对整体水肿肺进行通气会增加表面张力,这应会增加应力集中,并通过正反馈导致通气损伤不断加剧。在局部模型中,当压力屏障适中时,加速放气会使液体从充盈的肺泡中逸出并更均匀地重新分布。充盈的异质性趋于降低。在整体模型中,加速放气会使液体逸出,但由于表面张力升高,液体会跳到附近的通气肺泡中。充盈的异质性未改变。在表面张力正常的肺水肿中,早期采用加速放气进行通气可能会减少通气损伤随时间增加的正反馈机制。我们在离体大鼠肺中引入了一种表面张力升高的肺水肿新模型。我们首先产生静水压性水肿,然后轻柔地通气以增加表面张力。我们研究了(1)通气损伤水肿肺的力学机制以及(2)加速放气通气可能减轻通气损伤的机制。