Abstract
The thoracic wall provides the major retraction force for the liquid filled fetal lung. This could assist the movement of air into the lung at birth. The tone of the respiratory muscles in utero may set intrapulmonary pressure levels and facilitate movement of tracheal fluid out of the lungs. Surface rather than elastic forces probably are most important in determining the static work of breathing in the newborn. The lung is a source of tracheal fluid, and possibly amniotic fluid, phospholipids. Albumin may be an important stabilizer of tracheal fluid phospholipids. The lung synthesizes tracheal fluid phospholipids rapidly. Phosphatidyl ethanolamine is probably an important precursor of lecithin and this conversion may take place within tracheal fluid itself. These studies confirm our previous findings that the first fraction obtained from the Sephadex separation of lung extracts contains the lung surfactant system and that lung surfactant is not lipoprotein. There is little transfer of lipids from the fetus to the ewe. Phospholipids probably are synthesized by brown adipose tissue in the fetus; lipids do not cross the fetal blood brain barrier. The implications of these studies to pathogenesis of the respiratory distress syndrome was discussed.
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