Günther A, Kalinowski M, Rosseau S, Seeger W
Department of Internal Medicine, Justus Liebig University, Giessen, Germany.
Am J Respir Cell Mol Biol. 1995 Dec;13(6):712-8. doi: 10.1165/ajrcmb.13.6.7576709.
Intra-alveolar clot formation is a common finding in acute and chronic inflammatory lung diseases. Incorporation of lipophilic surfactant components into a growing fibrin clot has recently been reported (Am. J. Respir. Cell Mol. Biol. 1993; 9:213-220). In the present study, we investigated the influence of such surfactant incorporation on the elastic properties and water permeability of the fibrin polymer. Thrombelastography and compaction experiments were employed for assessment of the elastic properties, and the permeability characteristics of the clot material were addressed in fibrin-packed columns. Two calf lung surfactant extracts (CLSE and Alveofact), Curosurf, and a synthetic phospholipid mixture (dipalmitoylphosphatidylcholine, phosphatidylglycerol, and palmitic acid at a ratio of 68.5:22.5:9 [wt/wt]) were used. The presence of surfactant did not affect the cleavage of fibrinopeptide A upon incubation of fibrinogen with thrombin (enzyme-linked immunosorbent assay technique). Similarly, kinetics and extent of factor XIII-induced covalent crosslinkage of the fibrin network remained unchanged in the presence of surfactant (sodium dodecyl sulfate polyacrylamide gel electrophoresis and D-Dimer quantification upon subsequent clot lysis). All surfactants, however, dose-dependently decreased the elastic modulus of the arising fibrin polymer. The maximal amplitude in thrombelastography was reduced, and the recovery of fluid after centrifugation of the fibrin clot increased. Fibrin clots embedding natural surfactant material displayed reduced permeability for saline as compared with control fibrin polymers. Subsequent washout of lipids from these clots with Triton X-100 resulted in increased hydraulic conductivity. This was accompanied by an increase in pore size, suggesting altered architecture of the fibrin matrix generated in the presence of surfactant.(ABSTRACT TRUNCATED AT 250 WORDS)
肺泡内血栓形成是急慢性炎症性肺部疾病中的常见表现。最近有报道称亲脂性表面活性剂成分会融入正在形成的纤维蛋白凝块中(《美国呼吸细胞与分子生物学杂志》,1993年;9:213 - 220)。在本研究中,我们调查了这种表面活性剂的融入对纤维蛋白聚合物弹性特性和水渗透性的影响。采用血栓弹力图和压实实验来评估弹性特性,并在纤维蛋白填充柱中研究凝块材料的渗透特性。使用了两种小牛肺表面活性剂提取物(CLSE和Alveofact)、珂立苏以及一种合成磷脂混合物(二棕榈酰磷脂酰胆碱、磷脂酰甘油和棕榈酸,比例为68.5:22.5:9 [重量/重量])。表面活性剂的存在并不影响纤维蛋白原与凝血酶孵育时纤维蛋白肽A的裂解(酶联免疫吸附测定技术)。同样,在表面活性剂存在的情况下,因子XIII诱导的纤维蛋白网络共价交联的动力学和程度保持不变(十二烷基硫酸钠聚丙烯酰胺凝胶电泳以及随后凝块溶解后的D - 二聚体定量)。然而,所有表面活性剂均以剂量依赖方式降低了形成的纤维蛋白聚合物的弹性模量。血栓弹力图中的最大振幅降低,纤维蛋白凝块离心后的液体回收率增加。与对照纤维蛋白聚合物相比,嵌入天然表面活性剂材料的纤维蛋白凝块对盐水的渗透性降低。随后用Triton X - 100从这些凝块中洗脱出脂质导致水力传导率增加。这伴随着孔径增大,表明在表面活性剂存在下生成的纤维蛋白基质结构发生了改变。(摘要截短至250字)