Effect of acute hypoxia on airway and vascular exchangeable lung water spaces in dogs.

To determine if alveolar hypoxia causes subclinical noncardiogenic pulmonary edema, we measured in 8 dogs the rebreathing pulmonary tissue volume (Vt) and the pulmonary extravascular water volume using the single-pass double-indicator dilution method. After baseline measurements, the dogs were ventilated with the lowest concentration of oxygen that would not cause left ventricular failure (9 to 13% O2). One to 6 h of hypoxia had no effect on Vt, but caused a reversible 38% fall in pulmonary extravascular lung water volume by the indicator method (p less than 0.01). The ratio of the extravascular to vascular volumes estimated from the relative peak heights of the 2 indicator dilution curves did not change with hypoxia, which implies that hypoxia caused a derecruitment of pulmonary blood vessels rather than a real decrease in extra-vascular lung water volume. This conclusion is supported by our rebreathing measurement of the airway exchangeable tissue volume, which is virtually independent of tissue perfusion, and which did not fall during hypoxia. To determine if this alteration in the pulmonary circulation can cause pulmonary edema when the cardiac output is increased, we opened a femoral artery to femoral vein shunt in 9 additional dogs during ventilation with 9 to 13% oxygen. Cardiac output increased over 50% but pulmonary edema developed in only 1 dog, the dog that also had the highest mean pulmonary artery pressure of the group (35 mmHg versus group mean of 26 mmHg during hypoxia). We conclude that 1 to 6 h of alveolar hypoxia in dogs consistently decreases the volume of perfused lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)