The permeability of the alveolar epithelium is considerably less than the capillary endothelium, although macromolecules can traverse the epithelial lining of alveoli. Knowledge of the contributions of potential surface domains within the epithelial glycocalyx and of the surfactant lining layer to the differences in epithelial and endothelial permeabilities across the air-blood barrier is not secure. Increased numbers of type I vesicles and depletion of type II lamellar bodies characterize the alveolar epithelium after the development of septal edema and alveolar flooding. The thick sides of the alveolar septa are the sites of interstitial fluid accumulation and of increased attenuation along the surface of type I cells in edematous lungs. The development of septal edema and alveolar flooding at 15°C, on the other hand, is not associated with increased vesicles or depletion of lamellar body contents. Thus, these concomitant cellular changes are not primarily associated with formation of alveolar edema but more likely are responses to the distension of the septal interstitium and alveoli. The type II cell response could signify an attempt to replenish the surface active phospholipids after alveolar flooding. The vesicular response could represent a cellular defense mechanism against excessive interstitial fluid accumulation by providing a pathway for the return of excess filtrate to the blood (via an expanded endothelial vesicle population) or to the alveolar hypophase layer. The increased vesicle population, on the other hand, could signify an initial cellular pathologic response, with subsequent coalescence of the more closely packed vesicles leading to the formation of cytoplasmic vacuoles and finally to epithelial disruption.
|Original language||English (US)|
|Journal||American Review of Respiratory Disease|
|Issue number||5 Suppl|
|State||Published - 1983|
All Science Journal Classification (ASJC) codes
- Pulmonary and Respiratory Medicine