Guyton A C, Taylor A E, Drake R E, Parker J C
Ciba Found Symp. 1976(38):77-100. doi: 10.1002/9780470720202.ch6.
Systems analyses are presented for several aspects of pulmonary fluid dynamics, especially those related to (1) transport of fluid between the pulmonary interstitial spaces and the alveoli, (2) the possibility of a mechanism for concentrating protein in the lymph vessels, and (3) the effects of very high resistance to fluid flow in the alveolar septal wall. The analysis of fluid transport between the interstitial space and the alveoli, assuming that there is no active secretory or active absorptive process, shows that the interstitial fluid pressure in the normal lung cannot be more positive than the fluid pressure in the alveoli. Since the surface tension of this fluid causes it to have a subatmospheric pressure, the calculated maximum pressure for interstitial fluid in the normal lung is about -2 mmHg (-0.266 kPa). At any pressure more positive than this the alveoli will fill with fluid. The systems analyses for concentrating protein in the pulmonary lymphatics and for the effects of high resistance to fluid flow in the alveolar septal wall offer possible explanations for very negative pressures of pulmonary interstitial fluid, even though calculations of the interstitial fluid pressure based on the assumption that the colloid osmotic pressure of pulmonary interstitial fluid is equal to the osmotic pressure of pulmonary lymph give estimated pressures of pulmonary interstitial fluid approaching 0 mmHg.
本文对肺流体动力学的几个方面进行了系统分析，特别是与以下方面相关的内容：（1）肺间质间隙与肺泡之间的液体运输；（2）淋巴管中蛋白质浓缩机制的可能性；（3）肺泡间隔壁对液体流动的极高阻力的影响。在假设不存在主动分泌或主动吸收过程的情况下，对间质间隙与肺泡之间的液体运输进行分析表明，正常肺中的间质液压力不可能比肺泡中的液体压力更正。由于这种液体的表面张力使其具有低于大气压的压力，因此正常肺中间质液的计算最大压力约为-2 mmHg（-0.266 kPa）。在任何比此更正的压力下，肺泡都会充满液体。对肺淋巴管中蛋白质浓缩以及肺泡间隔壁对液体流动的高阻力影响的系统分析，为肺间质液的极低压力提供了可能的解释，尽管基于肺间质液胶体渗透压等于肺淋巴渗透压的假设对间质液压力进行计算时，得出的肺间质液压力估计值接近0 mmHg。
