Conhaim R L, Harms B A
Department of Surgery, University of Wisconsin-Madison.
Microvasc Res. 1992 Jul;44(1):14-26. doi: 10.1016/0026-2862(92)90098-a.
We used a simplified two-pore filtration model to examine the effects of hypoproteinemia on lung and soft tissue lymph flux in awake sheep (n = 7). To induce hypoproteinemia, we subjected each animal to 3 days of batch plasmapheresis (6 units per day). Data were collected in near steady-state conditions, 15-18 hr following completion of the last plasmapheresis episode. At this time, plasma protein concentration had fallen by 34%, while lung and soft tissue lymph protein concentrations had fallen by 55 and 62%, respectively. Lung and soft tissue lymph flows increased 52 and 87%, respectively. The plasma-to-lymph osmotic pressure gradients for lung and soft tissue lymph were unchanged by protein depletion (soft tissue, 7.7 mm Hg; lung, 4.8 mm Hg). We applied these results to a heteropore model of the microvascular barrier that consisted of two types of pores: those which plasma proteins could not cross (sigma = 1) and those which proteins could cross without restriction (sigma = 0). We varied the proportion of small pores to large pores until the measured data fit a model in which the calculated microvascular hydrostatic pressures in normal and hypoproteinemic conditions were equal. This was based on the assumption that microvascular hydrostatic pressure did not change with plasma protein depletion. These conditions could be satisfied when the small pores accounted for 90% of total barrier porosity. According to the model, lymph flow increased in hypoproteinemia because of an increase in protein-free liquid flux through the large percentage of small pores; protein flux through the small percentage of large pores remained unchanged. The net result was an increase in lymph flow and a decrease in the lymph protein concentration. The model reproduced these changes even though the plasma-to-lymph osmotic pressure gradients were unchanged. We conclude that a simplified heteropore model can explain the effects of hypoproteinemia on lung and soft tissue lymph flux.
我们使用了一个简化的双孔过滤模型来研究低蛋白血症对清醒绵羊（n = 7）肺和软组织淋巴流量的影响。为诱导低蛋白血症，我们让每只动物连续3天进行批量血浆置换（每天6单位）。在最后一次血浆置换结束后15 - 18小时，于接近稳态的条件下收集数据。此时，血浆蛋白浓度下降了34%，而肺和软组织淋巴蛋白浓度分别下降了55%和62%。肺和软组织淋巴流量分别增加了52%和87%。蛋白质耗竭并未改变肺和软组织淋巴的血浆 - 淋巴渗透压梯度（软组织，7.7 mmHg；肺，4.8 mmHg）。我们将这些结果应用于微血管屏障的异孔模型，该模型由两种类型的孔组成：血浆蛋白不能通过的孔（σ = 1）和蛋白可无限制通过的孔（σ = 0）。我们改变小孔与大孔的比例，直到测量数据符合一个模型，即在正常和低蛋白血症条件下计算出的微血管静水压力相等。这是基于微血管静水压力不会随血浆蛋白耗竭而改变的假设。当小孔占总屏障孔隙率的90%时，这些条件可以得到满足。根据该模型，低蛋白血症时淋巴流量增加是因为通过大部分小孔的无蛋白液体通量增加；通过小部分大孔的蛋白通量保持不变。最终结果是淋巴流量增加而淋巴蛋白浓度降低。即使血浆 - 淋巴渗透压梯度未改变，该模型也重现了这些变化。我们得出结论，一个简化的异孔模型可以解释低蛋白血症对肺和软组织淋巴流量的影响。
