Rebound increase in fetal breathing movements after 24 hour
prostaglandin e2 infusion in fetal sheep.
Hollingworth, S. A., S. A. Jones, and S. L. Adamson.
Program in Development and Fetal Health, Samuel Lunenfeld Research
Institute, Mount Sinai Hospital, 600 University Avenue, Toronto,
Ontario, Canada, M5G 1X5
APStracts 2:0403A, 1995.
We investigated the hypothesis that the precipitous decrease in
prostaglandin E2 (PGE2), a potent inhibitor of fetal breathing, from
high plasma concentrations during labour causes a rebound stimulation
of breathing before newborn concentrations have fallen below pre
-labour fetal values. Fetal plasma PGE2 concentration was gradually
increased from 384 +/- 82 (SE) pg/ml in 2 h steps (0 (baseline), 1.5,
3, 6 [mu]g/min) to labour levels (1230 +/- 381 pg/ml at 6 [mu]g/min)
and then was maintained for 24 h (n=9). PGE2 at 1.5 [mu]g/min
significantly decreased breathing incidence (42 +/- 4% (baseline) to
14 +/- 4%) and breath amplitude (2.1 +/- 0.5 to 1.5 +/- 0.2 arb.
units) and increased breath-breath interval (1.16 +/- 0.07 s to 1.56
+/- 0.06 s). No further dose-related changes were observed. During
the first 2 h after stopping PGE2 infusion, PGE2 concentration
returned to basal (352 +/- 64 pg/ml) but breathing incidence and
amplitude were significantly higher (74 +/- 8% and 2.4 +/- 0.3 arb.
units respectively) and breath-breath interval significantly lower
(0.95 +/- 0.10 s) than basal levels. Changes arose within nearly
equal to 15 min and were maintained for at least 4 h. Breathing did
not change significantly in the saline-treated group (n=7). Results
suggest that the rapid decrease in plasma PGE2 concentration at birth
promotes the onset of breathing.
Received 26 April 1995; accepted in final form 30 August 1995.
APS Manuscript Number A455-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.