Ontogeny of embryonic chicken lung: effects of pituitary gland, corticosterone, and other hormones upon pulmonary growth and synthesis of surfactant phospholipids

The actions of hormones on growth, cellular proliferation, and on synthetic rates of the major surfactant phospholipids, phosphatidylcholine (PC) and disaturated PC (DSPC), were studied in the lung of the chick embryo. Particular emphasis was placed on the effects of hypophysectomy, pituitary transplantation, and treatment with corticosterone (CORT). One study was concerned with hydrocortisone (HYCORT), estrogen (E2), thyroxine (T4), ovine prolactin (oPRL), and insulin. Hypophysectomy interfered with the normal gain in protein, the progressive dehydration of the embryonic lung, and also caused a reduction in the number of pulmonary cells on Days 16 and 18 of incubation. Absence of the pituitary gland diminished pulmonary PC by Day 16. Transplantation of one pituitary gland or exogenous CORT partially restored pulmonary phospholipid and PC (normalized per wet weight) in hypophysectomized (hypox) embryos. Transplantation also restored relative protein content in lungs of hypox individuals. Beyond this, transplantation was generally ineffective in reversing deficits of hypox individuals. All concentrations of CORT administered (30-100-300 micrograms) reduced the rate of pulmonary cell division. The highest dose was toxic as judged by its capacity to cause cellular death. Treatment of intact chicken embryos with CORT or E2 for two days stimulated incorporation of [14C]choline into PC and DSPC (the most surface-active component of PC) in the lungs of Day 17 embryos. CORT, but not E2, stimulated DSPC synthesis when treatment was increased to 3 days. Other hormones tested (T4, oPRL, insulin, and HYCORT) had no effect upon the rate of incorporation of [14C]choline into PC or DSPC. These results indicate that during ontogeny the avian lung becomes sensitive to CORT, and possibly E2, prior to 16 days of incubation. CORT, in particular, acts both to trigger the prehatching stimulation of surfactant phospholipid synthesis, especially the vital DSPC fraction, and to slow the rate of pulmonary cellular division coincident with biochemical differentiation of the surfactant system.