We have induced acute pulmonary oedema in upright anaesthetized dogs by increasing pulmonary microvascular permeability or by extracellular fluid volume overload in order to determine the sensitivity and specificity of the radiograph to the presence of abnormal lung water. Radiographs were taken before and after development of oedema. At the end of the experiment we removed the inflated lungs and froze them in liquid nitrogen and subsequently examined them macroscopically in the frozen state. The extravascular water/dry lung weight ratio was measured gravimetrically on seven portions of each lung. Finally without the base-line films for comparison. We directly measured the change in opacity of the films with a radiographic densitometer. When a dog's mean extravascular water/g dry lung was increased by more than 35% it was invariably recognized, in one or more zones, as definite oedema. Control dogs were reliably recognized as normal when base-line films were used but the distinction between normal and minor degrees of oedema could not be made without the base-line films. There was a positive correlation between radiological grade and lung water, but a great deal of overlap between grades. Densitometry was not a sensitive or reliable method for diagnosing or quantifying oedema. Oedema was usually associated with a decrease in volume of the lower lung zones.

In spontaneously breathing dogs (n = 8), maintained in the upright position, bronchial luminal diameter was measured from tantalum bronchograms. Changes in total intrathoracic lung volume were measured from radiographs taken at functional residual capacity (FRCR). With cooling of the cervical vagi to 0-4 degrees C mean bronchial diameter increased to 117 +/- 15 (SD)% of baseline diameter and FRCR increased to 113 +/- 16 of baseline volumes respectively. There was a significant correlation between changes in FRCR and bronchial diameter. After the vagi were rewarmed, pulmonary oedema was induced by rapid intravenous infusion of Hartmann's solution. Bronchi narrowed to a mean of 86 +/- 9% of baseline calibre and FRCR decreased (mean = 95 +/- 15%). With vagotomy bronchial diameter increased (mean = 102 +/- 12% of baseline diameter) but FRCR did not change significantly. Excluding one dog with gross oedema, changes in bronchial diameter due to oedema correlated positively with changes in FRCR; after vagotomy the relationship between diameter and FRCR was similar to that seen after vagal cooling in the baseline state, though individual values were lower. The shift in the diameter-FRCR relationship with vagotomy demonstrates that the direct bronchoconstrictor effect of the vagus is approximately doubled in the presence of pulmonary oedema. Bronchial and peribronchial oedema does not appear to directly narrow the bronchial lumen.

1.In dogs that were supported in the upright position and that were breathing spontaneously acute pulmonary oedema was induced either by extracellular fluid volume expansion (n = 5) or by increasing pulmonary microvascular permeability with alloxan (n = 5).2. Before oedema was induced, the bronchi of the right lung were outlined with tantalum powder.3. During a baseline period, standard chest radiographs were taken at inflation pressures from 0 to 2 kPa and the distributions of perfusion (with radioactive microspheres) and ventilation (with 133Xe) were measured. Arterial and mixed venous blood samples were taken to estimate the degree of venous admixture (physiological shunt) and pulmonary arterial and wedge pressures were measured. 4. After oedema had developed the radiographs and observations were repeated at a time when the pulmonary vascular pressures were insignificantly different from the baseline state.5. With induction of oedema, particularly when due to volume expansion, the lower-lung zones decrease in volume. There were no significant changes in the upper zones.6. Abnormal venous admixture occurred only in dogs with >20% loss of lower-zone volume; volume loss and physiological shunt were significantly correlated.7. The distribution of perfusion changed little with induction of oedema. Volume-expanded dogs showed a slight diversion of perfusion away from the bases and towards the upper zones.8. There was an approximately 30% reduction of ventilation to the lung bases and a corresponding increase to the upper zones. 9. With induction of oedema, bronchi were narrowed when there was a reduction of lung volume. There was a significant linear correlation between volume change and narrowing.

We measured the regional distribution of pulmonary extravascular and interstitial water to examine the possibility that regional differences in microvascular pressure or tissue stress may cause regional differences in lung water. We placed chloralose-anesthetized dogs in an upright (n = 6) or supine (n = 7) position for 180 min. We injected 51Cr-labeled EDTA to equilibrate to the extracellular space and 125I-labeled albumin to equilibrate with plasma. At the end of the experiment, the lungs were removed, passively drained of blood, and inflated before rapid freezing. Lungs were divided into horizontal slices, and extravascular, interstitial, and plasma water, red cell volume, and dry lung weight were determined for each slice. We found that regional extravascular and interstitial water were constant throughout the lungs in both groups and that there were no significant differences between upright and supine dogs. There were no significant differences in hematocrit between slices. We conclude that gravity and body position have no measurable effect on either the total size of the extravascular and interstitial compartments or their regional distribution.

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