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Decrease in plasma prostaglandin E2 is not essential for the establishment of continuous breathing at birth in sheep.

D S Lee1, P Choy, M Davi

  • 1Department of Pediatrics and Biochemistry, University of Manitoba, Winnipeg, Canada.

Journal of Developmental Physiology
|September 1, 1989
PubMed
Summary
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Indomethacin-induced continuous breathing in fetal sheep did not alter fetal behavior. Postnatal prostaglandin E2 (PGE2) levels were higher during breathing, suggesting PGE2 is not key to establishing breathing at birth.

Area of Science:

  • Fetal Physiology
  • Neonatal Respiration
  • Prostanoid Signaling

Background:

  • Indomethacin suppresses prostanoid concentrations, inducing continuous breathing in fetal sheep.
  • The association between indomethacin-induced breathing, fetal behavior, and prostaglandin E2 (PGE2) levels remains unclear.

Purpose of the Study:

  • To investigate if indomethacin-induced fetal breathing changes behavior.
  • To examine the relationship between PGE2 concentration changes and the onset of continuous breathing post-delivery.

Main Methods:

  • Infusion of indomethacin in fetal sheep to decrease PGE2.
  • Measurement of fetal and carotid arterial PGE2 concentrations.
  • Observation of fetal behavior and breathing patterns.

Related Experiment Videos

Main Results:

  • Indomethacin decreased fetal PGE2 levels, inducing continuous breathing without altering fetal wakefulness.
  • Postnatal continuous breathing began at higher PGE2 concentrations (1245 pg/ml) than those during fetal breathing activity (422 pg/ml).

Conclusions:

  • Prostaglandin E2 (PGE2) does not appear to be the primary factor in establishing continuous breathing at birth.
  • Fetal behavior is not directly linked to indomethacin-induced continuous breathing via PGE2 reduction.