Department of Physiology, Osijek Medical Faculty, Osijek, Croatia.
Med Hypotheses. 2010 Jun;74(6):993-9. doi: 10.1016/j.mehy.2010.01.018. Epub 2010 Feb 12.
The main puzzle of the pulmonary circulation is how the alveolar spaces remain dry over a wide range of pulmonary vascular pressures and blood flows. Although normal hydrostatic pressure in pulmonary capillaries is probably always below 10 mmHg, well bellow plasma colloid pressure of 25 mmHg, most textbooks state that some fluid filtration through capillary walls does occur, while the increased lymph drainage prevents alveolar fluid accumulation. The lack of a measurable pressure drop along pulmonary capillaries makes the classic description of Starling forces unsuitable to the low pressure, low resistance pulmonary circulation. Here presented model of pulmonary fluid traffic describes lungs as a matrix of small vascular units, each consisting of alveoli whose capillaries are anastomotically linked to the bronchiolar capillaries perfused by a single bronchiolar arteriole. It proposes that filtration and absorption in pulmonary and in bronchiolar capillaries happen as alternating periods of low and of increased perfusion pressures. The model is based on three levels of filtration control: short filtration phases due to respiratory cycle of the whole lung are modulated by bidirectional bronchiolo-pulmonar shunting independently in each small vascular unit, while fluid evaporation from alveolar groups further tunes local filtration. These mechanisms are used to describe a self-sustaining regulator that allows optimal fluid traffic in different settings. The proposed concept is used to describe development of pulmonary edema in several clinical entities (exercise in wet or dry climate, left heart failure, people who rapidly move to high altitudes, acute cyanide and carbon monoxide poisoning, large pulmonary embolisms).
肺循环的主要难题是肺泡空间如何在广泛的肺血管压力和血流范围内保持干燥。尽管肺毛细血管的静水压力通常可能低于 10mmHg，远低于 25mmHg 的血浆胶体渗透压，但大多数教科书都指出，毛细血管壁确实会发生一些液体滤过，而增加的淋巴引流则防止肺泡液体积聚。由于肺毛细血管缺乏可测量的压力下降，经典的 Starling 力描述不适合低压、低阻力的肺循环。这里提出的肺液流动模型将肺描述为小血管单元的基质，每个小血管单元由其毛细血管与单个细支气管小动脉灌注的细支气管毛细血管吻合的肺泡组成。它提出，肺毛细血管和细支气管毛细血管的滤过和吸收是通过低灌注压和高灌注压交替期发生的。该模型基于三个水平的滤过控制：整个肺的呼吸周期引起的短滤过相由每个小血管单元中独立的双向细支气管-肺分流调节，而肺泡群的液体蒸发则进一步调节局部滤过。这些机制用于描述允许在不同环境下实现最佳液体流动的自维持调节器。所提出的概念用于描述几种临床实体（湿或干气候下的运动、左心衰竭、迅速转移到高海拔地区的人、急性氰化物和一氧化碳中毒、大的肺栓塞）中肺水肿的发展。
