Intra-amniotic endotoxin accelerates lung maturation in fetal rabbits.

Abstract

The hypothesis that endotoxin in amniotic fluid accelerates fetal lung maturation was tested. On day 25 of gestation, LPS (5 microg/fetus) was injected intra-amniotically into one uterine horn of eight New Zealand white rabbits, whereas the contralateral amniotic sacs were injected with saline vehicle. The fetuses were delivered 48 h after LPS administration and their lungs were studied. One dam went into premature labor prior to the 48 h time point and was excluded from the study. Mean white cell counts in amniotic fluid and bronchoalveolar lavage fluid from LPS-treated fetuses were increased 3.2-fold (p = 0.04) and 9.9-fold (p = 0.04), respectively. Fetal weights and lung weights were not affected by LPS. Surfactant protein SP-A and SP-B mRNA expressions in LPS-treated fetuses were increased 2.3-fold (p = 0.03) and 1.4-fold (p = 0.04), respectively. Static lung compliance was increased in animals treated with LPS (p = 0.001). Lungs from LPS-treated animals had better aeration than those of controls. Mean volume of inflation-fixed lungs of LPS-treated fetuses was 1.7 times greater than that of controls (p = 0.03). Intra-uterine exposure to LPS increases surfactant protein expression and improves lung stability and aeration in preterm animals.