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Meclofenamate does not affect lung development in fetal sheep.
L D Wallen1, D T Murai, R I Clyman
1Cardiovascular Research Institute, San Francisco, California.
Journal of Developmental Physiology
|August 1, 1989
Summary
Prostaglandin E2 (PGE2) does not appear to drive fetal lung development changes before birth. Studies show inhibiting PGE2 did not alter tracheal fluid or surfactant production in fetal sheep.
Area of Science:
- Fetal Physiology
- Pulmonary Development
- Prostaglandin Biology
Background:
- Prostaglandins, particularly PGE2, are hypothesized to influence fetal lung development.
- Elevated fetal plasma PGE2 concentrations correlate with decreased tracheal fluid and increased surfactant production before delivery.
Purpose of the Study:
- To investigate if increased plasma PGE2 concentration is responsible for pre-delivery fetal lung maturation changes.
- To determine the role of PGE2 in regulating tracheal fluid production and surfactant metabolism in fetal sheep.
Main Methods:
- Continuous infusion of meclofenamate (prostaglandin synthetase inhibitor) in 8 fetal sheep.
- Control group received solvent infusion (5 fetal sheep).
- Measurements included plasma PGE2, tracheal fluid production, cortisol, surfactant, and lung tissue composition.
Main Results:
- Meclofenamate significantly reduced plasma PGE2 concentrations in treated fetal sheep.
- No significant effects of meclofenamate on tracheal fluid production, surfactant levels, or lung development markers were observed.
- Fetal plasma cortisol concentration and lung organ weights remained unaffected.
Conclusions:
- The typical increase in fetal plasma PGE2 before delivery is not essential for regulating tracheal fluid production or surfactant changes.
- Fetal lung development and maturation processes occurring before birth are independent of the usual high fetal PGE2 levels.