Two methods for the measurement of pulmonary edema are compared. The first method, which permits serial measurements in vivo, depends on the difference in mean transit time of a water label and an intravascular label. The second method is a postmortem one in which total lung water is measured and allocated to the pulmonary blood or to pulmonary extravascular water. Three groups of six dogs each were studied: controls, a group with pulmonary edema produced by elevating pulmonary venous pressure, and a group with pulmonary edema produced by alloxan. The isotopic as compared with the postmortem method accounted for 71% of the pulmonary extravascular water found in the controls, 94% in high pressure edema and 57% in alloxan edema. Shunting, as measured by a large fall in PaO 2 despite 100% oxygen breathing, became marked in a second group of five alloxan dogs and only 31% of the postmortem pulmonary extravascular water was measured by the isotope method. It is concluded that the isotope transit time method is a useful one for the serial measurement of pulmonary edema in vivo. The edema water is determined more accurately when pulmonary edema is due to elevated pulmonary venous pressure than when due to increased vascular permeability.

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We attempted to measure sodium and water spaces in the lungs before and after pulmonary edema produced in dogs by increasing pulmonary capillary pressure or by alloxan. We employed a technique depending on the difference in transit times through the lungs of tritiated water or 24 Na + , with reference to an intravascular indicator. In the control measurements, there was virtually complete recovery of the sodium indicator, but in pulmonary edema there was a significant loss. It is possible that this represents distribution of some of the 24 Na + into an extra vascular volume with an exit other than the pulmonary veins, but we would expect this to be accompanied by an equivalent amount of tritiated water. Since there was complete recovery of tritiated water in pulmonary edema, it seems more likely that the sodium loss represents binding by some extravascular locus and may be related to the extent of alveolar wall injury.ADDITIONAL KEY WORDS dogs sodium space water space alloxan isotope labeling• An interesting quality of the pulmonary alveolar wall is its relative impermeability to sodium ion as compared with water. This and other permeability characteristics of the pulmonary blood gas barrier have been extensively reviewed by Chinard (1). Relative impermeability to sodium is the case whether the ion is introduced into the pulmonary blood stream or is put into the conducting airways and detected in the blood flowing from the lung. It seems unlikely that this represents a peculiar quality of the alveolar capillary wall itself; it is more likely related to the intimate relationship of the capillary endothelium to the overlying alveolar epithelial layer which From the makes up part of the pathway. Taylor and associates (2) have measured the permeability coefficients of various substances in isolated perfused lung lobes and have found a value for sodium similar to values published for other living cellular membranes. We investigated permeability of the alveolar wall to sodium and water in experimental pulmonary edema because an increase in permeability to sodium ion might provide the basis for a better technique for quantifying pulmonary edema than the tritiated water method we have used previously (3, 4). An increased permeability to sodium ion could be detected since the sodium space would become significantly larger than the intravascular space and would approach the size of the extravascular water space. If the sodium space was not detectably greater than the simultaneously measured intravascular space, the osmotic forces of sodium and other ions would have to be added to those of the plasma proteins to keep the lungs free of edema. However, if there was an apparent loss of the sodium indicator, the sodium space

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