Johnson A, Blumenstock F A, Hussain M, Malik A B
Am J Pathol. 1984 Mar;114(3):410-7.
Sheep were prepared with lung lymph fistulas for assessment of the effects of complement activation on pulmonary transvascular fluid and protein exchange in the intact animal. Cobra venom factor (CVF 200 +/- 46 U/kg) was injected intravenously for activation of the complement system. In some animals (n = 6), pulmonary lymph flow (Qlym) and pulmonary arterial pressure (Ppa) increased without a change in the lymph-to-plasma protein concentration ratio (L/P) or in pulmonary blood flow (QL), indicating an increase in pulmonary vascular permeability to proteins. In another group (n = 6), Qlym and the L/P did not change, and there were also no changes in Ppa and QL following a similar injection of CVF. Morphologic evidence showed that leukocytes were trapped in pulmonary vessels and interstitium of both groups. Pulmonary edema was also present in both groups. Complement activation does not uniformly increase pulmonary lymph flow despite pathologic evidence of leukocyte sequestration and pulmonary edema. The lack of change in lymph flow in some animals may be due to lymphatic insufficiency, or lack of generation of humoral mediators, and/or a decrease in pulmonary capillary pressure.
通过制备羊肺淋巴瘘来评估补体激活对完整动物肺血管跨膜液体和蛋白质交换的影响。静脉注射眼镜蛇毒因子（CVF 200±46 U/kg）以激活补体系统。在一些动物（n = 6）中，肺淋巴流量（Qlym）和肺动脉压（Ppa）增加，而淋巴与血浆蛋白浓度比（L/P）和肺血流量（QL）无变化，表明肺血管对蛋白质的通透性增加。在另一组（n = 6）中，注射类似剂量的CVF后，Qlym和L/P未改变，Ppa和QL也无变化。形态学证据显示，两组动物的肺血管和间质中均有白细胞滞留。两组均出现肺水肿。尽管有白细胞隔离和肺水肿的病理证据，但补体激活并不一定会使肺淋巴流量均匀增加。部分动物淋巴流量无变化可能是由于淋巴功能不全、体液介质生成不足和/或肺毛细血管压降低。
