Drake R E, Laine G A, Allen S J, Katz J, Gabel J C
Center for Microvascular and Lymphatic Studies, University of Texas Medical School, Houston 77030.
Microvasc Res. 1987 Jul;34(1):96-107. doi: 10.1016/0026-2862(87)90082-3.
Our model of the pulmonary interstitial-lymphatic system is based on the assumption that the lung interstitial space can be divided into two compartments. The first compartment (C1) contains the terminal lymph vessels. Increases in the fluid pressure within this compartment, along with increased pressure generated by lymph vessel pumping, cause the lymph flow rate to increase. The lymph vessels run through the second compartment (C2) which we believe represents the perivascular spaces. Increases in the fluid volume of C2 cause the lymph vessels to dilate and this causes lymph vessel resistance to decrease. Normally the lymph flow rate equals the microvascular filtration rate so that lung fluid volume is constant. According to our model, increases in filtration rate cause fluid to collect in C1 and C2. The resulting increase in fluid pressure in C1, increased lymph vessel pumping, and the decrease in lymph vessel resistance in C2 cause lymph flow to increase. Eventually, the lymph flow rises to equal the filtration rate and lung fluid volume becomes constant again. The results of simulations with our model indicate that decreases in lymph vessel resistance are essential for lymph flow to increase substantially as edema develops.
我们的肺间质 - 淋巴系统模型基于这样一种假设，即肺间质空间可分为两个腔室。第一个腔室（C1）包含终末淋巴管。该腔室内流体压力的增加，以及淋巴管泵血产生的压力增加，会导致淋巴流速增加。淋巴管贯穿第二个腔室（C2），我们认为它代表血管周围间隙。C2中液体量的增加会导致淋巴管扩张，进而使淋巴管阻力降低。正常情况下，淋巴流速等于微血管滤过率，因此肺液体积保持恒定。根据我们的模型，滤过率增加会导致液体在C1和C2中积聚。C1中由此产生的流体压力增加、淋巴管泵血增加以及C2中淋巴管阻力降低，会导致淋巴流量增加。最终，淋巴流量上升至等于滤过率，肺液体积再次保持恒定。我们模型的模拟结果表明，随着水肿的发展，淋巴管阻力降低对于淋巴流量大幅增加至关重要。
