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The effects of plasma lavage on pulmonary surfactant and edema were studied in anesthetized open-chest dogs. After instrumentation and baseline measurements, citrated autologous plasma (1.5 ml/kg) was lavaged into each lung (n = 6). A control group was administered the same dose of buffered saline solution (n = 4). Hemodynamic parameters, blood gases, and lung compliance were monitored for 2 hours after lavage. Surfactant function, assessed with a Wilhelmy balance, and extravascular lung water measured gravimetrically were determined at the end of the experiment. Immediately after plasma lavage, a nonsegmental atelectasis was observed on the lung surface. Little change was seen in vascular pressures or cardiac output in either group, whereas partial pressure of oxygen in arterial blood and static compliance fell significantly after plasma lavage. Two hours after lavage, a large amount of white foam was observed in both large and small airways in the plasma group. Plasma but not saline lavage elevated surface tension minimum in pulmonary tissue. Airway foam contained functional surfactant; addition of plasma to normal surfactant on the Wilhelmy balance did not inhibit surfactant function. Extravascular lung water was increased in the plasma compared with the saline lavage group. These data suggest that plasma usurps surfactant from the alveolar hypophase rather than inhibiting its ability to lower surface tension. Because little change was measured in vascular pressures and it is unlikely that autologous plasma increases vascular permeability, we conclude that the edema was the result of high alveolar surface tension.

Inhalation injury occurs in 21% of flame burn victims who require large fluid volumes for resuscitation and have a mortality rate greater than 30%. This study was done to determine how vulnerable the smoke-injured lung is to fluid accumulation when crystalloids are infused rapidly. Mongrel dogs were exposed to smoke and 10% body-weight Ringer's lactate in three groups: (I) fluid only, (II) smoke only, and (III) smoke and fluid. The increase in wet-dry lung weight ratio was 2% in Group I, 28% in Group II, and 42% in Group III, consistent with pulmonary edema present only in Group III. The decrease in colloid oncotic pressure was similar in both of the groups that were given fluid, and the rise in the surface tension minimum of lung extracts was similar in both of the groups that were exposed to smoke. The smoke-injured lung loses the ability to protect itself when challenged with fluid. Reduced oncotic pressure is not responsible. Changes in microvascular pressure, endothelial and epithelial damage, and surfactant inactivation interact to cause this increase in extravascular lung water.