Lai-Fook S J
Crit Rev Biomed Eng. 1986;13(3):171-200.
Recent research in pulmonary physiology, anatomy, and mechanics have clarified our general understanding of liquid and solute transport through the lung. Fluid crosses the microvascular endothelial membrane at a rate that depends on gradients in the transmembrane hydrostatic and osmotic pressures and the conductance of the permeable membrane. Under normal conditions, the filtered fluid is removed by an efficient lymphatic pump. Edema accumulates in the lung when an increased flux due to an elevated vascular pressure or to a more permeable membrane is not matched by an adequate lymph clearance rate. Initially a favorable hydrostatic pressure gradient drives the excess fluid into interstitial spaces surrounding large blood vessels and airways away from filtration sites near capillaries and thereby ensures efficient gas exchange. Further edema formation reduces the pressure gradient, eventually leading to the flooding of alveolar air spaces and impaired gas exchange. I will focus on the role of the above forces in the regulation of extravascular lung water. It will become clear that many details of the general scheme are not known, and our conceptual understanding of the relevant mechanisms involved is often rudimentary and incomplete. Some of the more important questions pertain to the interstitial pressure around capillaries, the resistance and compliance of the interstitial matrix, and the role of the lymphatics in regulating interstitial fluid volume and interstitial pressure.
近期在肺生理学、解剖学和力学方面的研究，已使我们对液体和溶质在肺内的转运有了更全面的认识。液体穿过微血管内皮膜的速率取决于跨膜静水压和渗透压的梯度以及可渗透膜的传导性。在正常情况下，滤过的液体由高效的淋巴泵清除。当由于血管压力升高或膜通透性增加导致的液体通量增加，而淋巴清除率不足时，肺水肿就会在肺内积聚。最初，有利的静水压梯度将多余的液体驱入围绕大血管和气道的间质间隙，远离毛细血管附近的滤过部位，从而确保有效的气体交换。进一步的水肿形成会降低压力梯度，最终导致肺泡气腔被液体充满，气体交换受损。我将重点关注上述作用力在调节血管外肺水方面的作用。很明显，总体机制的许多细节尚不清楚，我们对相关机制的概念性理解往往是初步且不完整的。一些更重要的问题涉及毛细血管周围的间质压力、间质基质的阻力和顺应性，以及淋巴管在调节间质液体积和间质压力中的作用。
