Ultrastructure of the pulmonary alveolar septa after hemodynamic edema

Increased numbers of micropinocytotic vesicles were observed in cells of the air-blood barrier of isolated dog lungs after increased filtration from the microcirculation had created septal edema and alveolar flooding. In studies of dog lungs in vivo, increased rates of filtration from the microcirculation were not associated with increased numbers of cellular vesicles. Since extravascular fluid accumulation in these studies was restricted to the extraalveolar connective tissue spaces, alveolar septal edema and potentially associated increases in alveolar interstitial tissue pressures also failed to occur. Even though the specific sites of increased filtration from the pulmonary microcirculation were not determined, these results are consistent with the interpretation that fluid accumulation in the alveolar septa does not occur until pulmonary lymphatic capacity is overcome. Furthermore, increased cellular vesiculation, which was observed in the isolated lung studies only after septal edema had developed, was not associated with increased filtration but was more likely a response to distension of the septal interstitium. Accordingly, the increased number of vesicles could represent a cellular defense mechanism against excessive interstitial fluid accumulation by providing a pathway for the return of excess filtrate to the blood and alveolar surfaces. The expanded vesicular population, on the other hand, could signify an initial cellular pathologic response, with subsequent coalescence of the more closely packed vesicles eventually leading to the formation of cytoplasmic vacuoles and ultimately to disruption of the lining cell layers.