Prostaglandin E2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

1998 ◽  
Vol 76 (9) ◽  
pp. 858-866 ◽  
Author(s):  
Carole S Watson ◽  
Jacobus H Homan ◽  
Susan E White ◽  
John R Challis ◽  
Alan D Bocking
Keyword(s):  
Blood Flow ◽  
Ethanol Exposure ◽  
Late Gestation ◽  
Prostaglandin E ◽  
Uterine Blood Flow ◽  
Fetal Plasma ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Baseline Incidence ◽  
And Control

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E2 (PGE2) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE2]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE2] 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 PGE2 is also diminished during RUBF. PGE2 (594 ± 19 ng·min-1·kg-1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO2 = 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 PGE2 increased plasma [PGE2] 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 PGE2 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 PGE2. We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE2 may be a result of an alteration in brainstem receptor function or number or local PGE2 removal.Key words: fetal breathing movements, prostaglandin E2, hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

Prostaglandin E2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

1998 ◽  
Vol 76 (9) ◽  
pp. 858-866
Author(s):  
Carole S. Watson ◽  
Jacobus H. Homan ◽  
Susan E. White ◽  
John R. Challis ◽  
Alan D. Bocking
Keyword(s):  
Blood Flow ◽  
Prostaglandin E ◽  
Uterine Blood Flow ◽  
Fetal Breathing ◽  
Fetal Breathing Movements

Fetal endocrine responses to prolonged hypoxemia in sheep

1990 ◽  
Vol 259 (4) ◽  
pp. R703-R708 ◽  
Author(s):  
S. B. Hooper ◽  
C. L. Coulter ◽  
J. M. Deayton ◽  
R. Harding ◽  
G. D. Thorburn
Keyword(s):  
Blood Flow ◽  
Time Course ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Plasma Norepinephrine ◽  
Uterine Blood Flow ◽  
Fetal Plasma ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Fetal Breathing Movements

Our aim was to characterize the pattern of release of epinephrine, norepinephrine, arginine vasopressin (AVP), cortisol (hydrocortisone), and prostaglandin E2 (PGE2) into the fetal circulation during prolonged reductions in uterine blood flow (RUBF). In five sheep RUBF was induced for 24 h, whereas in another five sheep (controls) uterine blood flow was not reduced. Fetal arterial oxygen saturation was decreased from 60.5 +/- 3.6 to 20.3 +/- 1.6% after 2 h of RUBF and remained significantly reduced for the entire RUBF period. The incidence of fetal breathing movements (FBM) and fetal arterial pH were reduced from 36.7 +/- 4.5 min/h and 7.36 +/- 0.01 to 4.3 +/- 1.8 min/h and 7.13 +/- 0.02, respectively, after 2 h of RUBF, but both had returned to control levels after 14 h. Fetal plasma AVP and epinephrine concentrations were increased from 4.4 +/- 0.5 pg/ml and 0.19 +/- 0.05 ng/ml to 333.8 +/- 41.5 pg/ml and 1.5 +/- 0.6 ng/ml, respectively, after 2 h and then declined to near control levels after 12 h of RUBF. Fetal plasma norepinephrine and cortisol concentrations were increased from 1.3 +/- 0.4 and 4.0 +/- 2.2 ng/ml to 6.1 +/- 1.8 and 13.5 +/- 4.1 ng/ml, respectively, after 2 h of RUBF, and both remained significantly elevated throughout the remainder of the RUBF period. Fetal plasma PGE2 concentrations progressively increased (from 1.9 +/- 0.4 to 8.8 +/- 1.7 nmol/l at 12 h) as the duration of RUBF increased and were still significantly elevated after 24 h. The time course for the increase in PGE2 during RUBF was very similar to the increases in arterial pH and in the incidence of FBM.(ABSTRACT TRUNCATED AT 250 WORDS)

Behavioral activity during prolonged hypoxemia in fetal sheep

1988 ◽  
Vol 65 (6) ◽  
pp. 2420-2426 ◽  
Author(s):  
A. D. Bocking ◽  
R. Gagnon ◽  
K. M. Milne ◽  
S. E. White
Keyword(s):  
Blood Flow ◽  
Eye Movements ◽  
Normal Incidence ◽  
Behavioral Activity ◽  
Uterine Blood Flow ◽  
Fetal Sheep ◽  
Pregnant Sheep ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Internal Iliac

Experiments were conducted in unanesthetized, chronically catheterized pregnant sheep to determine the fetal behavioral response to prolonged hypoxemia produced by restricting uterine blood flow. Uterine blood flow was reduced by adjusting a vascular occluder placed around the maternal common internal iliac artery to decrease fetal arterial O2 content from 6.1 +/- 0.3 to 4.1 +/- 0.3 ml/dl for 48 h. Associated with the decrease in fetal O2 content, there was a slight increase in fetal arterial PCO2 and decrease in pH, which were both transient. There was an initial inhibition of both fetal breathing movements and eye movements but no change in the pattern of electrocortical activity. After this initial inhibition there was a return to normal incidence of both fetal breathing movements and eye movements by 16 h of the prolonged hypoxemia. These studies indicate that the chronically catheterized sheep fetus is able to adapt behaviorally to a prolonged decrease in arterial O2 content secondary to the restriction of uterine blood flow.

Effects of restricting uteroplacental blood flow on concentrations of corticotrophin-releasing hormone, adrenocorticotrophin, cortisol, and prostaglandin E2 in the sheep fetus during late pregnancy

1992 ◽  
Vol 70 (10) ◽  
pp. 1396-1402 ◽  
Author(s):  
Alicia Sue-Tang ◽  
Alan D. Booking ◽  
A. Nigel Brooks ◽  
Stuart Hooper ◽  
Susan E. White ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Vein ◽  
Arterial Oxygen Saturation ◽  
Control Level ◽  
Arterial Oxygen ◽  
Prostaglandin E ◽  
Uterine Blood Flow ◽  
Concentration Difference ◽  
Releasing Hormone ◽  
Fetal Plasma

We have examined the effects of reduced uterine blood flow and prolonged fetal hypoxemia on the temporal relationship between changes in hormones associated with the activity of the pituitary–adrenal axis (corticotrophin-releasing hormone (CRH), adrenocorticotrophin (ACTH), cortisol, and prostaglandin E2 (PGE2)) in the ovine fetus at 120–125 days of pregnancy, and we sought evidence for placental secretion of CRH and ACTH during prolonged hypoxemia. Uterine blood flow was reduced by placing an adjustable Teflon clamp around the maternal common internal iliac artery to decrease fetal arterial oxygen saturation from mean values of 59.1 ± 3.3 to 25.7 ± 4.6% (±SEM, n = 10). There was a transient peak in immunoreactive (IR-) CRH at 1–2 h after reducing uterine blood flow. IR-ACTH rose to peak values at +2 h, then gradually decreased to control level by +12 h. Fetal plasma cortisol and PGE2 concentrations were elevated significantly by +2 and +4 h, respectively, and at 20–24 h. The identity of IR-CRH in fetal plasma and in ovine placental extracts was confirmed by HPLC, but there was no consistent umbilical vein – femoral arterial concentration difference for either IR-CRH or IR-ACTH during normoxemia or hypoxemia. We conclude that a sequence of endocrine changes involving CRH, ACTH, PGE2, and cortisol occurs in the fetus during a prolonged reduction in uterine blood flow. However, we did not obtain evidence, for placental secretion of either CRH or ACTH in response to this manipulation.Key words: fetus, adrenocorticotrophin, corticotrophin-releasing hormone, prostaglandin E2, placenta.

Fetal breathing is not inhibited by ethanol exposure during prolonged reduced uterine blood flow

1996 ◽  
Vol 74 (9) ◽  
pp. 1016-1024 ◽  
Author(s):  
C S Watson ◽  
S E White ◽  
J Homan ◽  
S Abdollah ◽  
J F Brien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ethanol Exposure ◽  
Uterine Blood Flow ◽  
Fetal Breathing

Effects of meclofenamate on breathing movements in fetal sheep before delivery

1988 ◽  
Vol 64 (2) ◽  
pp. 759-766 ◽  
Author(s):  
L. D. Wallen ◽  
D. T. Murai ◽  
R. I. Clyman ◽  
C. H. Lee ◽  
F. E. Mauray ◽  
...  
Keyword(s):  
Low Voltage ◽  
Late Gestation ◽  
Fetal Sheep ◽  
Electrocortical Activity ◽  
Fetal Plasma ◽  
Prostaglandin Synthase ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Synthase Inhibitor ◽  
Control Infusion

There is evidence that prostaglandins (PG), specifically PGE2, participate in the regulation of fetal breathing movements (FBM). During late gestation, when FBM occur intermittently and primarily during low-voltage electrocortical activity, the concentration of PGE2 in fetal plasma ([PGE2]) is high. During the days before delivery [PGE2] increases and FBM decrease. To determine whether the increase in [PGE2] is responsible for the concurrent decrease in FBM, we infused the prostaglandin synthase inhibitor, meclofenamate (0.7 mg.kg-1.h-1), into eight fetal sheep continuously for 5-–13 days before delivery; five control fetuses received a continuous infusion of the solvent for 5–11 days before delivery. Compared with control infusion, meclofenamate caused a significant decrease in [PGE 2] until the day of delivery and a significant increase in FBM [overall and during high-voltage electrocortical activity (HVA)] until 2 days before delivery. Although there were significant correlations between [PGE2] and FBM (overall and during HVA), both groups showed similar decreases in FBM during the 2 days before delivery. We conclude that the decrease in FBM before delivery is not dependent on the concurrent increase in [PGE2].

Rebound increase in fetal breathing movements after 24-h prostaglandin E2 infusion in fetal sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 166-175 ◽  
Author(s):  
S. A. Hollingworth ◽  
S. A. Jones ◽  
S. L. Adamson
Keyword(s):  
Prostaglandin E2 ◽  
Plasma Concentrations ◽  
Treated Group ◽  
High Plasma ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Pge2 Concentration ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Rebound Increase

We investigated the hypothesis that the precipitous decrease in prostaglandin E2 (PGE2), a potent inhibitor of fetal breathing, from high plasma concentrations during labor causes a rebound stimulation of breathing without newborn concentrations falling below prelabor fetal values. Fetal plasma PGE2 concentration was gradually increased from 384 +/- 82 (SE) pg/ml in 2-h steps [0 (baseline), 1.5, 3, and 6 micrograms/min] to labor levels (1,230 +/- 381 pg/ml at 6 micrograms/min) and then was maintained for 24 h (n = 9). PGE2 at 1.5 micrograms/min significantly decreased breathing incidence [from 42 +/- 4 (baseline) to 14 +/- 4%] and breath amplitude (from 2.1 +/- 0.5 to 1.5 +/- 0.2 arbitrary units) and increased breath-to-breath interval (from 1.16 +/- 0.07 to 1.56 +/- 0.06 s). No further dose-related changes were observed. During the first 2 h after PGE2 infusion was stopped, PGE2 concentration returned to basal (352 +/- 64 pg/ml) but breathing incidence and amplitude were significantly higher (74 +/- 8% and 2.4 +/- 0.3 arbitrary units, respectively) and breath-to-breath interval was significantly lower (0.95 +/- 0.10 s) than were basal levels. Changes arose within approximately 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.

487 Effect of melatonin supplementation during mid- to late-gestation on maternal uterine blood flow and calf size at birth

2017 ◽  
Vol 95 (suppl_4) ◽  
pp. 238-238
Author(s):  
K. J. McCarty ◽  
M. P. T. Owen ◽  
C. G. Hart ◽  
K. C. Yankey ◽  
R. C. Thompson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Late Gestation ◽  
Uterine Blood Flow ◽  
Size At Birth

Uterine blood flow and substrate uptake in conscious rabbit during late gestation

1984 ◽  
Vol 247 (5) ◽  
pp. E574-E580 ◽  
Author(s):  
M. Gilbert ◽  
S. Hauguel ◽  
M. Bouisset
Keyword(s):  
Blood Flow ◽  
Ketone Bodies ◽  
Glucose Consumption ◽  
Late Gestation ◽  
Gravid Uterus ◽  
Glucose Turnover ◽  
Substrate Uptake ◽  
Uterine Blood Flow ◽  
Fourfold Increase ◽  
Fick Principle

The aim of this study was the quantitation of the metabolic demands of the uterus in rabbits between days 24 and 30 of gestation, a time at which there is a fourfold increase in fetal weight. Serial measurements of substrate concentrations in maternal artery and uterine vein were performed over this period. Uterine blood flow was measured on days 24 and 30. Uterine substrate uptake was calculated by application of the Fick principle. Over the gestation range studied, the absolute uterine blood flow increased proportionally to the uterine weight gain. The uterine arteriovenous differences for glucose (G), lactate (L), free fatty acids (FFA), ketone bodies (KB), and oxygen (O2) were constant throughout the study. At both gestational ages, the weight-specific uterine substrate consumption (G, FFA, KB, O2) and production (L) were respectively similar. On days 24 and 30 the amount of G directed to the gravid uterus represented approximately 13 and approximately 36% of the maternal glucose turnover rate, respectively. The maximum contributions of G and FFA to the uterine oxygen consumption on day 24 were 80 and 30%, respectively. We have thus confirmed that at term the gravid uterus is a site of high glucose consumption. Finally, we demonstrated that in a nonruminant species, FFA would be a substantial source of carbon.

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