Increased lung vascular permeability after arachidonic acid and hydrostatic challenge

AND HEINZ NEUHOF. Increased lung vascular permeability after arachidonic acid and hydrostatic challenge. J. Appl. Physiol. 61(5): 1781-1789, 1986.-Arachidonic acid (AA) metabolites are known to be potent vasoactive substances in the pulmonary circulation, whereas their influence on lung vascular permea-bility is still uncertain. We investigated the effect of AA bolus injection on the capillary filtration coefficient (&c) of isolated rabbit lungs, recirculatingly perfused with Krebs-Henseleit al-bumin (1%) buffer. Kf c was measured using repetitive sudden venous pressure elevations (7.5 Torr) and time zero extrapola-tion of the slope of the weight gain curve. It ranged from 1.3 to 2.4 cm3. s-l l Torr-l l g-l l 10m4 in control lungs. Pulmonary arte-rial injection of AA (100 PM; in presence of 20 PM indometh-acin to suppress pulmonary arterial pressure rise) during an acute hydrostatic challenge, but not at zero venous pressure, caused a>10-fold increase in &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. capillary filtration coefficient; hydraulic conductivity; vascular compliance; indomethacin; isolated rabbit lung OXYGENATION PRODUCTS of arachidonic acid (AA) are known to produce local inflammatory reactions in many organs ( 11). In extrapulmonary tissues sulfidopeptide leukotrienes have been shown to cause increased capil-lary permeability (for review see Refs. 12, 23). In the pulmonary circulation AA products were found to be potent vasoactive substances, which increase (endoper-oxides, thromboxane, prostaglandin Fza, sulfidopeptide leukotrienes) or decrease (prostaglandin 12) the pulmo