Seeger W, Walmrath D, Menger M, Neuhof H
J Appl Physiol (1985). 1986 Nov;61(5):1781-9. doi: 10.1152/jappl.1986.61.5.1781.
Arachidonic acid (AA) metabolites are known to be potent vasoactive substances in the pulmonary circulation, whereas their influence on lung vascular permeability is still uncertain. We investigated the effect of AA bolus injection on the capillary filtration coefficient (Kf,C) of isolated rabbit lungs, recirculatingly perfused with Krebs-Henseleit albumin (1%) buffer. Kf,C was measured using repetitive sudden venous pressure elevations (7.5 Torr) and time zero extrapolation of the slope of the weight gain curve. It ranged from 1.3 to 2.4 cm3 X s-1 X Torr-1 X g-1 X 10(-4) in control lungs. Pulmonary arterial injection of AA (100 microM; in presence of 20 microM indomethacin to suppress pulmonary arterial pressure rise) during an acute hydrostatic challenge, but not at zero venous pressure, caused a greater than 10-fold increase in Kf,C. Vascular compliance was not altered. Additional experiments, performed under zero-flow conditions to avoid any ambiguity in microvascular pressure, corroborated the severalfold increase in vascular permeability, detectable within 3 min after AA application during acute hydrostatic challenge.
已知花生四烯酸（AA）代谢产物是肺循环中强效的血管活性物质，但其对肺血管通透性的影响仍不确定。我们研究了在 Krebs-Henseleit 白蛋白（1%）缓冲液再循环灌注的情况下，静脉推注 AA 对离体兔肺毛细血管滤过系数（Kf,C）的影响。Kf,C 通过重复突然升高静脉压力（7.5 托）并对体重增加曲线斜率进行零时间外推来测量。在对照肺中，其范围为 1.3 至 2.4 cm³×s⁻¹×托⁻¹×g⁻¹×10⁻⁴。在急性流体静压挑战期间（而非静脉压力为零时），肺动脉注射 AA（100 μM；同时存在 20 μM 吲哚美辛以抑制肺动脉压力升高）导致 Kf,C 增加超过 10 倍。血管顺应性未改变。在零流量条件下进行的额外实验，以避免微血管压力出现任何模糊性，证实了在急性流体静压挑战期间应用 AA 后 3 分钟内可检测到血管通透性增加数倍。
