[Pharmacological influences on fetal lung maturity, part V: Influencing the pulmonary DPL (dipalmitoyl lecithin) level with L-thyroxin (T4)]

Dipalmitoyl lecithin (DPL = DPPC, dipalmitoyl phosphatidyl choline) is both quantitatively and functionally the most important constituent of the surfactant complex. The effect of thyroxin (T4) on fetal lung maturity was investigated by means of selective DPL determination. Following administration of thyroxin to the mother animal an increase in the DPPC content was demonstrated in rat fetuses. This increase was greater than that of the total phospholipids. This effect of thyroxin could be due to the following causes: 1, Earlier and accelerated differentiation of lung cells: more Type II cells are formed earlier and these synthesize DPPC more effectively than other lung cells (approx. 40-50% of the phosphocoline in Type II cells in DPPC). 2. Stimulation of the deacylation-reacylation cycle. 3. A combination of these mechanisms.