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  • Title: Extra-alveolar vessel contribution to hydrostatic pulmonary edema in in situ dog lungs.
    Author: Albert RK, Lakshminarayan S, Charan NB, Kirk W, Butler J.
    Journal: J Appl Physiol Respir Environ Exerc Physiol; 1983 Apr; 54(4):1010-7. PubMed ID: 6853276.
    Abstract:
    We determined the relative contribution of larger extra-alveolar arteries and veins to hydrostatic edema in in situ dog lungs. Left lower lobe alveolar and vascular pressures were controlled in 24 open-chest, anesthetized, heparinized dogs. Zero pressure was at the lobe base. Normal blood gases were maintained by ventilating the right lung. The left lower lobe was inflated with 5% CO2 and air to an alveolar pressure of 10 or 25 cmH2O and suspended from a strain gauge, which allowed continual weight recording. Vascular pressures were raised to alveolar pressure plus lung height (zone III) before and after pulmonary arterial or venous embolization with 37- to 74-microns polystyrene beads, which isolated the larger extra-alveolar arteries or veins from alveolar vessels. The weight change occurring during the last 3 min of the 5-min hydrostatic stress was taken to represent transvascular fluid flux. At an alveolar pressure of 25 cmH2O (estimated transmural pressure 40 cmH2O), leakage from the larger extra-alveolar arteries and veins accounted for 41 and 32%, respectively, of the total transvascular fluid flux occurring after embolization. At an alveolar pressure of 10 cmH2O (estimated transmural pressure 22 cmH2O), no extra-alveolar vessel leakage occurred. However, when vascular pressures were raised to provide a transmural pressure similar to that present at the higher alveolar pressure, the same contribution from larger extra-alveolar vessels was observed.
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