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Intra‐amniotic endotoxin accelerates lung maturation in fetal rabbits
Author(s) -
Bry Kristina,
Lappalainen Urpo
Publication year - 2001
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2001.tb00259.x
Subject(s) - medicine , fetus , amniotic fluid , lung , bronchoalveolar lavage , andrology , gestation , saline , endocrinology , pregnancy , biology , genetics
The hypothesis that endotoxin in amniotic fluid accelerates fetal lung maturation was tested. On day 25 of gestation, LPS (5 μg/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). Conclusion: Intra‐uterine exposure to LPS increases surfactant protein expression and improves lung stability and aeration in preterm animals.