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J Appl Physiol 54: 1010-1017, 1983;
8750-7587/83 $5.00
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Journal of Applied Physiology, Vol 54, Issue 4 1010-1017, Copyright © 1983 by American Physiological Society

ARTICLES

Extra-alveolar vessel contribution to hydrostatic pulmonary edema in in situ dog lungs

R. K. Albert, S. Lakshminarayan, N. B. Charan, W. Kirk and J. Butler

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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