Fetal Rat Lung Development: Lipids and Surface Tension Properties After Decapitation in utero 1

Abstract

Summary

Decapitation in utero produces hormonal deficiencies which do not influence lung organogenesis but retards pneumocyte differentiation at the organelle and molecular levels. Such lungs contain decreased quantities of phospholipid and functionally are impaired in their ability to reduce surface tension to normal levels. The mechanisms by which these alterations are produced are most likely related to hormonal deficiencies during fetal development. These deficiencies may specifically alter lung phospholipid metabolism. Retardation of phospholipid metabolism may, however, be secondary to a more generalized retardation of pneumocyte differentiation. We favor the latter hypothesis in so far as pituitary failure occurring in man and animals with fully mature lungs does not lead to clinical respiratory distress (33, 38). Further inquiry into the manner in which hormones influence lung metabolism will require evaluation of the effect of specific hormonal replacements on in utero decapitated or hypophysectomized fetuses and on lung explants differentiating in vitro.