The Surfactant System in the Lung of the Embryonic and Juvenile Chicken: Biochemical, Ultrastructural, and Endocrine Studies.

Abstract

Maturation of the pulmonary surfactant system and its endocrine control were investigated in the embryonic and post-hatchng chicken. Growth and maturation of the chicken lung were examined morphologically and biochemically. The capability of lung slices of day 14 and day 19 embryos to incorporate ('14)C-choline or ('14)C-glucose into the two most important phospholipids in surfactant, phosphatidylcholine (PC) and disaturated phosphatidylcholine (DSPC) was determined. Effects of the pituitary, corticosterone (CORT), and other hormones upon pulmonary growth, maturation, and synthetic rates of PC and DSPC were also studied. Maturation of the avian lung occurred in three stages. Prior to day 14, few air spaces were present, hydration was prominent, and cell division occurred at a slow rate. After day 14, parabronchi increased in number concomitant with increased accumulation of DNA. Content of glucose, water, and glycogen, originally high on day 14, decreased thereafter. By 18 days of incubation, well-developed and numerous parabronchi and blood capillaries replaced mesenchyme. After day 18, air capillaries appeared and cellular division slowed coincident with increased numbers of lamellar bodies and content and synthesis of pulmonary PC and DSPC. DSPC was uniquely enriched in the embroynic lung compared with yolk or liver. Most PC and DSPC was in isolated lamellar bodies and pulmonary lavage. Analysis of fatty acids of DSPC revealed that 85% was dipalmitoyl PC. Incorporation of ('14)C-choline into PC and DSPC was higher in lungs of chicken embryos just prior to breathing (day 19) compared with younger embryos (day 14). In contrast, the rate of incorporation of ('14)C-glucose into these phosphoglycerides was reduced on day 19 compared to day 14. Hypophysectomy reduced growth and PC in the embryonic lung. Replacement of a pituitary or administration of CORT restored pulmonary content of PC (expressed per wet weight). CORT and 17-(beta)-estradiol stimulated incorporation of ('14)C-choline into PC and DSPC of day 17 embryonic lungs. Stimulation depended upon time and duration of administration. High doses of CORT slowed pulmonary cell division and caused cellular death; lower doses of CORT only reduced cell division. The avian lung is similar to the mammalian lung in many aspects of composition, biosynthesis, and regulation of phospholipids related to surfactant.Ph.D.Animal PhysiologyUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/158850/1/8215019.pd