FETAL MOUSE LUNG ULTRASTRUCTURAL MATURATION IS ACCELERATED BY MATERNAL THYROTROPIN-RELEASING-HORMONE TREATMENT

Maternal administration of thyrotropin-releasing hormone, alone or in combination with corticosteroid, accelerates functional, morphologic a nd biochemical fetal lung maturation. However, the dose-response relat ionship of maternal thyrotropin-releasing hormone treatment and accele ration of fetal lung ultrastructural maturation or disaturated phospha tidylcholine content has not been investigated. We administered (i.p.) saline or thyrotropin-releasing hormone (0.2, 0.4 or 0.6 mg/kg/dose) to the pregnant Balb/c mouse on days 16 and 17 (b.i.d.) and on day 18 of gestation (1 h prior to killing). Morphometric ultrastructural anal ysis and quantitation of disaturated phosphatidylcholine content was d one on the 18-day gestation fetal lung. Maternal thyrotropin-releasing hormone treatment resulted in an increase in the number of lamellar b odies and depletion of glycogen in fetal lung type II cells, and an in crease in the lung airspace to parenchymal ratio. In addition, a strik ing difference in the pattern of lung growth was noted in the thyrotro pin-releasing-hormone-treated (0.4 and 0.6 mg/kg/dose) groups. These l ungs had larger air spaces, thinner alveolar septae and more air-blood barriers. Maternal thyrotropin-releasing hormone treatment did not in fluence fetal lung disaturated phosphatidylcholine content. We conclud e that in the mouse, maternal thyrotropin-releasing hormone treatment enhances fetal lung structural maturation and propose that thyrotropin -releasing hormone plays a role in mammalian fetal lung growth.