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Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep
Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep
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Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep
Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

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Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep
Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep
Journal Article

Prostaglandin E 2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

1998
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Overview
Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E 2 (PGE 2 ) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE 2 ]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE 2 ] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE 2 is also diminished during RUBF. PGE 2 (594 ± 19 ng·min -1 ·kg -1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO 2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO 2 = 22 ± 1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE 2 increased plasma [PGE 2 ] from 881 ± 162 to 1189 ± 114 pg·mL -1 in RUBF fetuses and from 334 ± 72 to 616 ± 118 pg·mL -1 (p < 0.05) in control fetuses. FBM were initially inhibited by PGE 2 from 22.5 ± 9.4 and 17.9 ± 6.5% of the time to 6.9 ± 2.4 and 0.5 ± 0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE 2 . We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE 2 may be a result of an alteration in brainstem receptor function or number or local PGE 2 removal.Key words: fetal breathing movements, prostaglandin E 2 , hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

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