Acute and Subacute Effects of Injury on the Canine Alveolar Septum: Results (9)

Assuming that repair processes have not kept pace with injury, the development of through-and-through septal gaps (ie, pores and fenestrae) might produce more rapid airspace enlargement if they occurred at septal junctions rather than in the alveolar wall between junctions. Retraction of the edges of a gap at the junction of three alveolar walls might lead to coalescence of three adjacent airspaces, rather than just two, as in the case of a fenestration in the septum between two alveolar airspaces. Whether this mechanism is operative in the experimental animal or in man is, of course, not yet known.
Another hypothesis suggested by these findings is that alveolar junctional sites are especially vulnerable to injury, and are therefore also the principle loci of regeneration or repair. Increased injury at alveolar wall junctions may be due to the surface tension characteristics of the peripheral lung, which may have produced a higher concentration of the agent producing lung damage in the alveolar corners. Such might be the case for any injurious agent which entered the alveolar surface lining through the airways.
Finally, the striking increase in prevalence of through-and-through gaps in the alveolar septum occupied by type 2 cells in the two-week specimen coupled with the in vitro studies cited makes it conceivable that this cell may play a role in the repair of the alveolar septum which goes beyond that of merely replacing injured type 1 cells.

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