Seeger W, Wolf H, Stähler G, Neuhof H, Róka L
Klin Wochenschr. 1981 May 4;59(9):459-61. doi: 10.1007/BF01695900.
Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.
花生四烯酸的释放和代谢被认为是不同刺激作用于肺血管内皮细胞的共同最终途径。在一个离体、通气和灌注的兔肺模型中，我们研究了游离花生四烯酸可用性增加对肺血管阻力和通透性的影响。向灌注液中添加花生四烯酸或通过钙离子载体A 23187释放花生四烯酸，通常会使肺血管阻力出现特征性的双相增加以及通透性持续增加，随后出现肺水肿。吲哚美辛抑制环氧化酶可防止血管阻力增加，但血管通透性的增加却会增强。因此，肺血管阻力的升高可归因于环氧化酶产物，而肺血管通透性的增加则归因于花生四烯酸的脂氧合酶产物。
