INFLUENCE OF POSTNATALLY ADMINISTERED GLUCOCORTICOIDS ON RAT LUNG GROWTH

Postnatal formation of alveoli can be largely prevented by glucocortic oid treatment, which accelerates alveolar wall thinning and inhibits o utgrowth of new interalveolar septa. Since a double capillary network is a prerequisite for interalveolar wall formation, we hypothesized th at glucocorticoid treatment inhibited alveolar formation, indirectly, by inducing precocious microvascular maturation. Between 4 and 60 days we followed up qualitatively and quantitatively the effects of 2 week s (days 2-15) of daily Decadron(R) (Dexamethasone phosphate) injection s on the lung structure. Glucocorticoid induced only small changes in body weight or lung volume. However, during the first 2 weeks, it acce lerated alveolar wall thinning and microvascular maturation and partly suppressed the outgrowth of new interalveolar septa. In Decadron-trea ted rats, the interstitial tissue mass was significantly reduced durin g the first 2 weeks, and a larger alveolar surface area was endowed wi th a capillary monolayer on days 10 and 13. One week after drug withdr awal, the trend towards precocious maturation of the lung was reversed . Lipofibroblasts reappeared, and inter-airspace septa regressed towar ds a more immature state. We found indications of a second burst of al veolization by resumption of secondary septa formation. The late seque lae of Decadron treatment (day 60) were manifested as an 'emphysematou s' condition of the lungs, with larger and fewer airspaces, the delaye d alveolization being insufficient to compensate for the initial defic it.