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Updated: Aug 17, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
[Effect of intra-amnial thyroxine administration in the fetus]
Abstract:
Stimulation of the surfactant production in foetal lung cells by thyroxine has been shown in experiments on animals. In humans, too, thyroxine instilled intra-amnially should increase lung maturity. Therefore, amniotic fluid samples were taken from 22 women before the 35th week of gestation before instilling 500 micrograms levothyroxine and then during labour, and blood samples were taken half an hour and also 24 hours after instillation of thyroxine into the amniotic fluid and during labour. The concentration of thyroxine, triiodinethyronine and reversed triiodinethyronine were measured radioimmunologically in the amniotic fluid samples and blood samples, and the lecithin concentration was also determined enzymatically in the amniotic fluid samples. The occurrence of cases of membrane syndrome in the examined group, and the foetal heart rate were subsequently determined after thyroxine had been administered. The results showed that the foetus resorbed the thyroxine administered intra-amnially and--in a manner typical of foetal metabolism--converted it by preference to rT3. The thyroxine dosage leads to only a temporary increase in foetal thyroid gland hormones. The thyroxine given intra-amnially is not absorbed in considerable amounts by the mother. The lecithin content of the amniotic fluid was significantly increased after a dose of thyroxine, possibly a reversible increase. The membrane syndrome rate laid below the expected number; in 5 of the 22 cases a foetal tachycardia was observed about 2 days after thyroxine administration.
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