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KMID : 0381219810130010047
Journal of RIMSK
1981 Volume.13 No. 1 p.47 ~ p.53
The Effect of Glucocorticoid on Fetal Lung Maturation


Abstract
In the human, development of the lung is perhaps the most critical event determining the health and survival of prematurely delivered infants. Pulmonary immaturity, expressed as a deficiency of alveolar surfactant, is the major cause of idiopathic respiratiry distress syndrome (IRDS), or hyaline membrane disease, in premature infants.
In view of the effects of glucocorticoids on lungs of fetal animals, it has been proposed that administration of these hormones to the human fetus at risk for premature delivery might induce alveolar surfactant and prevent IRDS. In this regard, a benefical effects of treatment of mothers in premature labor with betamethasone, a potent synthetic glucocorticoid has recently been reported.
Glucocorticoids trigger specific developmental events in a number of Efetal and newborn tissues. It now appears that these hormones have a similar effect during development of the fetal lung. Administration of corticosteroids to fetal lambs or rabbits cause both acceleraed morphological development of the lung and precocious appearance of alveolar surfactant. Such treatment increase the survival rate for prematurely delivered animals.
Umbilical cord blood cortisol levels in neonates who subsquently developed hyaline membrane diseases were shown to be lower than those in normal newborns of comparable gestational age.
More recently, amniotic fluid cortisol levels were demonstrated to correlate well with the umbilical cord blood cortisol "concentratiop. A number of experimental and clinical trial involving both animal models and human subjects have concluden that antepartum glucocortiocid administration resulted in an acceleration of the process of fetal lung maturation and a decreased incidence of the respiratory distress syndrome. Moreover, significant correlation was observed between amniotic fluid cortisol, levels and the L/S ratios in uncomplicated pregnncy.
The earlist known event in the interaction of glucocorticoids with their target cell is the binding of steroid by specific ;cytoplasmic receptor proteins. The receptor hormone complex thus formed transfer to the nucleus, which it attaches to nuclear acceptor sites and presumably influences specific gene activity.
The detection of receptor in the lungs of fetal rabbits and lambs thus indicates that this organ is capable of responding to glucocorticoids and sggests that these hormones directly influence the lung during fetal life.
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