Brigham K L, Woolverton W C, Blake L H, Staub N C
J Clin Invest. 1974 Oct;54(4):792-804. doi: 10.1172/JCI107819.
In awake sheep, we compared the responses of lung lymph flow and lymph and plasma protein concentrations to steady state elevations of pulmonary vascular pressures made by inflating a left atrial balloon with those after an intravenous infusion of 10(5)-10(10)Pseudomonas aeruginosa. Lymph flow increased when pressure was increased, but lymph-plasma protein concentration ratios always fell and lymph protein flow (lymph flow x lymph protein concentration) increased only slightly. After Pseudomonas, sheep had transient chills, fever, leukopenia, hypoxemia, increased pulmonary artery pressure and lymph flow and decreased left atrial pressure and lymph protein concentration, 3-5 h after Pseudomonas, when vascular pressures and lymph protein concentrations had returned to near base line, lymph flow increased further to 3-10 times base line and remained at a steady level for many hours. During this steady state period, lymph-plasma protein concentration ratios were similar to base line and lymph protein flow was higher than in the increased pressure studies. Two sheep died of pulmonary edema 7 and 9 h after Pseudomonas, but in 16 studies, five other sheep appeared well during the period of highest lymph flow and all variables returned to base line in 24-72 h. Six serial indicator dilution lung water studies in five sheep changed insignificantly from base line after Pseudomonas. Postmortem lung water was high in the two sheep dead of pulmonary edema and one other, but six sheep killed 1-6 h after Pseudomonas had normal lung water. Because of the clear difference between the effects of increased pressure and Pseudomonas on lymphplasma protein concentration ratios and lymph protein flow, we conclude that Pseudomonas causes a prolonged increase in lung vessel permeability to protein. Because we saw lung lymph flow as high as 10 times base line without pulmonary edema, we conclude that lung lymphatics are a sensitive high-capacity mechanism for removing excess filtered fluid. An equivalent pore model of sheep lung vessels suggests that the changes we saw after Pseudomonas could result from small changes in the structure of exchanging vessel walls.
在清醒的绵羊中，我们比较了通过向左心房球囊充气使肺血管压力稳定升高时以及静脉注射10⁵ - 10¹⁰铜绿假单胞菌后肺淋巴流量、淋巴和血浆蛋白浓度的反应。压力升高时淋巴流量增加，但淋巴 - 血浆蛋白浓度比值总是下降，淋巴蛋白流量（淋巴流量×淋巴蛋白浓度）仅略有增加。注射铜绿假单胞菌后，绵羊出现短暂寒战、发热、白细胞减少、低氧血症、肺动脉压和淋巴流量增加以及左心房压和淋巴蛋白浓度降低，在注射铜绿假单胞菌3 - 5小时后，当血管压力和淋巴蛋白浓度恢复到接近基线水平时，淋巴流量进一步增加至基线的3 - 10倍，并在许多小时内保持稳定水平。在此稳定期，淋巴 - 血浆蛋白浓度比值与基线相似，淋巴蛋白流量高于压力升高研究中的情况。两只绵羊在注射铜绿假单胞菌后7小时和9小时死于肺水肿，但在16项研究中，另外五只绵羊在淋巴流量最高期间状况良好，所有变量在24 - 72小时内恢复到基线水平。对五只绵羊进行的六项连续指示剂稀释肺水研究在注射铜绿假单胞菌后与基线相比变化不显著。死于肺水肿的两只绵羊以及另一只绵羊死后肺水含量很高，但在注射铜绿假单胞菌后1 - 6小时处死的六只绵羊肺水含量正常。由于压力升高和铜绿假单胞菌对淋巴 - 血浆蛋白浓度比值和淋巴蛋白流量的影响存在明显差异，我们得出结论，铜绿假单胞菌会导致肺血管对蛋白质的通透性长时间增加。因为我们观察到肺淋巴流量高达基线的10倍而没有肺水肿，所以我们得出结论，肺淋巴管是清除过量滤过液的敏感且高容量机制。绵羊肺血管的等效孔模型表明，我们在注射铜绿假单胞菌后看到的变化可能是由于交换血管壁结构的微小变化所致。
