Extra-alveolar vessel contribution to hydrostatic pulmonary edema in in situ dog lungs.
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.
D000818:Animals; D001158:Arteries; D001808:Blood Vessels / Q000473:pathology; D001980:Bronchi / Q000098:blood supply; D004285:Dogs; D005260:Female; D006874:Hydrostatic Pressure; D008297:Male; D008863:Microspheres; D011650:Pulmonary Alveoli / Q000098:blood supply; D011651:Pulmonary Artery; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000503:physiopathology*; D011667:Pulmonary Veins; D014655:Vascular Resistance