Effect of prostaglandin E2 on ovine maternal placental blood flow

1976 ◽  
Vol 231 (3) ◽  
pp. 754-759 ◽  
Author(s):  
JH Rankin ◽  
TM Phernetton

The effect of PGE2 on regional blood flows in the chronically catheterized near-term pregnant sheep was investigated using radioactive microspheres. The injection of 20 mug PGE2 per kilogram into the left ventricle of eight sheep resulted in no change in maternal brain and noncotyledonary uterine flow. The renal blood flow increased from 692 to 892 ml/min (P less than 0.004). The uterine blood flow decreased from 673 to 317 ml/min (P less than 0.001). The trium was bypassed by injecting 7 mug PGE2 per kilogram of sheep into a fetal venous catheter and permitting it to reach the placental vasculature after placental transfer. Eleven sets of observations were made in eight animals. We observed no change in the intrauterine pressure, maternal brain flow, and noncotyledonary uterine blood flow secondary to this procedure. The maternal renal blood flow changed from 592 to 669 ml/min (P less than 0.007). The uterine blood flow increased from 762 to 853 ml/min (P less than 0.02). The uterine vascular resistance decreased from 0.124 to 0.115 mmHg x min/ml (P less than 0.04). It was concluded that 1) PGE3 crosses the placenta quite readily, and 2) PGE3 causes dilatation of the maternal placental vascular bed.

1989 ◽  
Vol 257 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
C. R. Rosenfeld ◽  
R. P. Naden

The uteroplacental vasculature is more refractory to angiotensin II (ANG II) than the systemic vasculature as a whole. To ascertain the differences in responses between reproductive and nonreproductive tissues that account for this, we infused ANG II (0.573, 5.73, and 11.5 micrograms/min) in pregnant sheep (137 +/- 5 days of gestation) and monitored arterial pressure (MAP), heart rate, and uterine blood flow (UBF); cardiac output and regional blood flows were measured with radiolabeled microspheres. Dose-dependent changes in MAP, UBF, and systemic (SVR) and uterine (UVR) vascular resistance occurred (P less than 0.05); systemic responses exceeded uterine (P less than 0.05), except with 11.5 micrograms/min, when % delta UVR = % delta SVR, % delta UVR greater than % delta MAP, and UBF fell 29%. Although a dose-dependent rise in placental resistance occurred, blood flow was unaffected except at 11.5 micrograms ANG II/min, falling 16.8 +/- 3.5% (P = 0.059). In contrast, endometrial perfusion decreased 68 +/- 4.2 and 81 +/- 1.8% (P less than 0.01) with 5.73 and 11.5 micrograms ANG II/min, respectively. Myometrial responses were intermediate, thus placental flow increased from 75 to greater than 90% of total UBF. Adipose, renal, and adrenal glands were extremely sensitive to ANG II, with blood flows decreasing maximally at 0.573 micrograms/min (P less than 0.05). Maximum adipose vascular resistance occurred at 0.573 micrograms/min, greater than 400% (P less than 0.001), exceeding responses in all tissues (P less than 0.05). The placenta is less responsive to ANG II than other uterine and most nonreproductive tissues, resulting in preferential maintenance of uteroplacental perfusion and protecting the fetus from the effects of this vasoconstrictor.


1976 ◽  
Vol 41 (5) ◽  
pp. 727-733 ◽  
Author(s):  
A. M. Walker ◽  
G. K. Oakes ◽  
R. Ehrenkranz ◽  
M. McLaughlin ◽  
R. A. Chez

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2–16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100–200 mg/kg. Mean fetal arterial Pco2 increased from49.5 to 63.4 mmHg but no significant changes in umbilical blood flowoccurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. Nodignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despitean increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistancedid not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor innormal physiological regulation of the uteroplacental circulation in this species.


1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.


1961 ◽  
Vol 16 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
N. S. Assali ◽  
L. Holm ◽  
H. Parker

The effects of oxytocin on regional blood flow and regional vascular resistance were investigated in a group of pregnant ewes and bitches not in labor and in another group in early labor. Single injections or intravenous drip infusion did not change significantly arterial pressure, cardiac output, electrocardiogram, and renal, iliac, femoral, and carotid blood flows in any of the animals studied. The effects on the pregnant uterus were negligible before the onset of spontaneous labor. Only when the animal was in labor did oxytocin produce an increase in uterine contractions accompanied by a significant decrease in uterine blood flow. The data indicate that in the pregnant sheep and dog the circulatory action of oxytocin is limited to the pregnant uterus in labor and that the decrease in blood flow is probably due to an increase in intramural vascular resistance caused by the contracting myometrium around the uterine arterioles. Submitted on May 5, 1961


1977 ◽  
Vol 5 (1) ◽  
pp. 39-55 ◽  
Author(s):  
Heinz-Dieter Junge ◽  
Wolfgang Künzel ◽  
Friedrich Karl Klöck

1974 ◽  
Vol 2 (2) ◽  
pp. 101-105 ◽  
Author(s):  
Wolfgang Künzel ◽  
Friedrich Karl Klöck ◽  
Heinz-Dieter Junge ◽  
Waldemar Moll

1988 ◽  
Vol 65 (6) ◽  
pp. 2420-2426 ◽  
Author(s):  
A. D. Bocking ◽  
R. Gagnon ◽  
K. M. Milne ◽  
S. E. White

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.


1982 ◽  
Vol 242 (3) ◽  
pp. H429-H436 ◽  
Author(s):  
R. B. Wilkening ◽  
S. Anderson ◽  
L. Martensson ◽  
G. Meschia

The effect of variations of uterine blood flow (F) on placental transfer was examined in six chronic sheep preparations by measuring the placental clearances of ethanol (CE) and antipyrine (CA) at different levels of F. Norepinephrine infusion, hemorrhage, and occlusion of the terminal aorta were used to reduce F below normal. The reduction of F had no appreciable effect on umbilical blood flow (f). In each ewe, CE significantly correlated with F. The CE vs. F relationship at constant f was curvilinear with convexity toward the clearance axis. Regression analysis showed that the equation 1/CE = 1/.911 F + 1/.831 f could account for most of the CE variance (r2 = 0.97). Implicit in this relation is the concept that, given a certain level of placental perfusion, an F/f ratio congruent to 1 is optimal for the exchange of highly diffusible inert molecules between mother and fetus [CE/(F + f) was maximum at F/f = 0.955]. CA was not significantly different from CE at low clearance level but became smaller than CE at clearance values greater than 300 ml/min. This suggests that a high rates of perfusion placental permeability was a factor in limiting CA.


1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.


PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1013-1014
Author(s):  
RAUL BEJAR

Baylen and Emmanouilides give the impression that their abstract was misquoted in our commentary. We would like to explain our interpretation of their data. In the abstract, Baylen et al indicate that they measured regional blood flows (RBF) in premature fetal lambs, expressing them as a percentage of the left ventricular output (LVO) before and after patent ductus arteriosus (PDA) closure. Their results (percent of LVO) before and after PDA closure were: lung, 42.7% vs 8.4% (P < .01); carcass, 35% vs 55% (P < .01); heart, 5.5% vs 10.2% (P < .05); gastrointestinal tract, 5.1% vs 9.3% (P < .05); brain, 2.7% vs 3.4% (P = NS); kidney, 2.2% vs 3.3% (P = NS); liver, 3.2% vs 5.7% (P = NS).


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