scholarly journals Erratum: Local delivery of VEGF adenovirus to the uterine artery increases vasorelaxation and uterine blood flow in the pregnant sheep

Gene Therapy ◽  
2008 ◽  
Vol 15 (20) ◽  
pp. 1410-1410
Author(s):  
A L David ◽  
B Torondel ◽  
I Zachary ◽  
V Wigley ◽  
K Abi-Nader ◽  
...  
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Local Delivery ◽  
Uterine Blood Flow ◽  
Pregnant Sheep

scholarly journals Local delivery of VEGF adenovirus to the uterine artery increases vasorelaxation and uterine blood flow in the pregnant sheep

Gene Therapy ◽  
2008 ◽  
Vol 15 (19) ◽  
pp. 1344-1350 ◽  
Author(s):  
A L David ◽  
B Torondel ◽  
I Zachary ◽  
V Wigley ◽  
K A Nader ◽  
...  
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Local Delivery ◽  
Uterine Blood Flow ◽  
Pregnant Sheep

Endogenous hormones and regulation of uterine blood flow during pregnancy

1986 ◽  
Vol 250 (3) ◽  
pp. R365-R369 ◽  
Author(s):  
D. Caton ◽  
P. S. Kalra
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Daily Variation ◽  
Correlation Coefficients ◽  
Endogenous Hormones ◽  
Uterine Blood Flow ◽  
Pregnant Sheep ◽  
Flow Through

Fourteen pregnant sheep were prepared for measurements of blood flow through a major uterine artery (UBF) and of arterial concentrations of estrone, estradiol, and progestagen. Five of the animals were ovariectomized. Measurements were made daily (n = 12) or every 4 h for 24 h (n = 4). Statistically significant (P less than 0.01) correlation coefficients were detected between UBF and hormone, either alone or in combination; the closest and most consistent associations were those in which estrogen and progestagen concentrations were summed or multiplied. Ewes with higher hormonal concentrations were those that had the higher rates of UBF. Correlation coefficients were statistically significant more often among ovariectomized animals. No associations were detected within one animal that delivered a growth-retarded fetus nor from any of the 24-h data. Estrogens and progestagen accounted for as much as 25% of the daily variation of UBF among and within sheep during the last half of pregnancy.

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.

Uterine artery pseudoaneurysm and embolisation during pregnancy

2020 ◽  
Vol 13 (5) ◽  
pp. e234058
Author(s):  
Jared T Roeckner ◽  
Adetola F Louis-Jacques ◽  
Bruce R Zwiebel ◽  
Judette M Louis
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Thrombin Injection ◽  
Uterine Blood Flow ◽  
Coil Embolisation ◽  
Artery Pseudoaneurysm ◽  
Healthy Young Woman ◽  
Dangerous Condition ◽  
Uterine Artery Pseudoaneurysm ◽  
In Pregnancy

Uterine artery pseudoaneurysm in pregnancy is a dangerous condition as rupture can be catastrophic due to the large volume of uterine blood flow. We present a case of a healthy, young woman with a desired pregnancy at 15 weeks of gestation incidentally discovered to have a pseudoaneurysm of the uterine artery during a routine prenatal ultrasound. She underwent initial thrombin injection followed by endovascular coil embolisation of the left uterine artery and carried the pregnancy to term without further complications.

Functional role of angiotensin II type 1 and 2 receptors in regulation of uterine blood flow in nonpregnant sheep

2000 ◽  
Vol 278 (2) ◽  
pp. H353-H359 ◽  
Author(s):  
Donna S. Lambers ◽  
Suzanne G. Greenberg ◽  
Kenneth E. Clark
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Uterine Artery ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Response Curves ◽  
Vascular Responses

The objective was to determine the receptor subtype of angiotensin II (ANG II) that is responsible for vasoconstriction in the nonpregnant ovine uterine and systemic vasculatures. Seven nonpregnant estrogenized ewes with indwelling uterine artery catheters and flow probes received bolus injections (0.1, 0.3 and 1 μg) of ANG II locally into the uterine artery followed by a systemic infusion of ANG II at 100 ng ⋅ kg−1 ⋅ min−1for 10 min to determine uterine vasoconstrictor responses. Uterine ANG II dose-response curves were repeated following administration of the ANG II type 2 receptor (AT2) antagonist PD-123319 and then repeated again in the presence of an ANG II type 1 receptor (AT1) antagonist L-158809. In a second experiment, designed to investigate the mechanism of ANG II potentiation that occurred in the presence of AT2 blockade, nonestrogenized sheep received a uterine artery infusion of L-158809 (3 mg/min for 5 min) prior to the infusion of 0.03 μg/min of ANG II for 10 min. ANG II produced dose-dependent decreases in uterine blood flow ( P < 0.03), which were potentiated in the presence of the AT2 antagonist ( P < 0.02). Addition of the AT1 antagonist abolished the uterine vascular responses and blocked ANG II-induced increases in systemic arterial pressure ( P < 0.01). Significant uterine vasodilation ( P < 0.01) was noted with AT1 blockade in the second experiment, which was reversed by administration of the AT2 antagonist or by the nitric oxide synthetase inhibitor N ω-nitro-l-arginine methyl ester. We conclude that the AT1- receptors mediate the systemic and uterine vasoconstrictor responses to ANG II in the nonpregnant ewe. AT2-receptor blockade resulted in a potentiation of the uterine vasoconstrictor response to ANG II, suggesting that the AT2-receptor subtype may modulate uterine vascular responses to ANG II potentially by release of nitric oxide.

The Effects of S(+)-Ketamine and Racemic Ketamine on Uterine Blood Flow in Chronically Instrumented Pregnant Sheep

2004 ◽  
pp. 497-502 ◽  
Author(s):  
Danja Str??mper ◽  
Wiebke Gogarten ◽  
Marcel E. Durieux ◽  
Kristian Hartleb ◽  
Hugo Van Aken ◽  
...  
Keyword(s):  
Blood Flow ◽  
Uterine Blood Flow ◽  
Pregnant Sheep ◽  
Racemic Ketamine

Effects of hyperthermia on uterine blood flow and shunting through uterine arteriovenous anastomoses in the late-pregnant ewe

1999 ◽  
Vol 11 (5) ◽  
pp. 201 ◽  
Author(s):  
Suzanne L. Miller ◽  
Graham Jenkin ◽  
David W. Walker
Keyword(s):  
Blood Flow ◽  
Experimental Period ◽  
Respiratory Alkalosis ◽  
Uterine Horn ◽  
Arteriovenous Anastomoses ◽  
Uterine Blood Flow ◽  
Ambient Conditions ◽  
Total Blood ◽  
Uterine Arteries ◽  
Pregnant Sheep

The effect of maternal hyperthermia on uterine blood flow (UBF) through the two main uterine arteries and on the proportion of UBF shunted through uterine arteriovenous anastomoses (AVAs) was investigated. Eight late-pregnant ewes were exposed to normothermic (22–23˚C) or hyperthermic (approx-imately 39˚C) ambient conditions for 8 h. UBF was measured in the left and right uterine arteries using flow probes and microspheres were injected into the uterine artery before, during and after the experimental period. The distribution of microspheres between the uterus and lungs was determined to calculate changes in capillary and AVA blood flows. Hyperthermia produced a significant (P<0.05) increase in maternal core temperature (+1.5˚C), increase in maternal blood pH (+0.21; P<0.05) and decrease in maternal pCO 2 (–16.2 mmHg; P<0.05). Blood flow to the uterine horn ipsilateral to the corpus luteum (CL) remained unchanged during hyperthermia, whereas total UBF and blood flow to the contralateral uterine horn were significantly decreased (P<0.05), by 23.1% and 20.8%, respectively, of pre-heat control values. The proportion of UBF shunted through uterine AVAs during hyperthermia was not significantly different from values observed in normothermic ewes (21.9 0.7%). Mild to moderate hyperthermia in late-pregnant sheep induces respiratory alkalosis and decreases total blood flow to the uterus, brought about by a decrease in blood flow to the uterine horn contralateral, but not ipsilateral to the CL. Heat treatment does not alter the proportion of UBF traversing uterine AVAs.

scholarly journals Large Conductance Ca2+-Activated and Voltage-Activated K+ Channels Contribute to the Rise and Maintenance of Estrogen-Induced Uterine Vasodilation and Maintenance of Blood Pressure

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6012-6020 ◽  
Author(s):  
Charles R. Rosenfeld ◽  
Timothy Roy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Uterine Artery ◽  
K Channel ◽  
Uterine Blood Flow ◽  
K Channels ◽  
Channel Inhibition ◽  
Estradiol 17Β ◽  
Cgmp Synthesis

Abstract Uterine blood flow (UBF) increases greater than 4-fold 90 min after systemic estradiol-17β (E2β) in nonpregnant sheep and remains elevated longer than 6–8 h; mean arterial pressure (MAP) is unchanged. Large-conductance Ca+2-activated (BKCa) and voltage-activated (KV) K+ channels contribute to the acute rise in UBF; their role in maintaining UBF and MAP longer than 90 min is unknown. We examined this in five nonpregnant, ovariectomized ewes with uterine artery (UA) flow probes and catheters in a UA for infusion of K+ channel inhibitors and uterine vein to sample venous effluent. Animals received systemic E2β (1.0 μg/kg; control), E2β+UA tetraethylammonium (TEA; 0.4–0.8 mm, n = 4), and E2β+UA 4-aminopyridine (4-AP; 0.01–0.08 mm, n = 4) to block BKCa and KV, respectively, while monitoring MAP, heart rate, and UBF. Uterine cGMP synthesis was measured. Ninety minutes after E2β, UBF rose 4.5-fold, uterine vascular resistance (UVR) fell greater than 5-fold and MAP was unchanged [78 ± 0.8 (sem) vs. 77 ± 1.5 mm Hg] in control studies and before UA inhibition with TEA and 4-AP. Between 90 and 120min, UBF, UVR, and MAP were unchanged after E2β alone. E2β+TEA dose dependently decreased ipsilateral UBF and increased UVR (24 ± 8.9 and 38 ± 16%, respectively, at 0.8 mm; P &lt; 0.03); MAP was unchanged. Contralateral UBF/UVR were unaffected. E2β+4-AP also dose dependently decreased ipsilateral UBF and increased UVR (27 ± 5.3 and 76 ± 18%, respectively, at 0.08 mm; P &lt; 0.001); however, MAP rose 27 ± 6.9% (P ≤ 0.006). E2β increased uterine cGMP synthesis greater than 3.5-fold and was unaffected by local K+ channel inhibition. BKCa and KV contribute to the rise and maintenance of E2β-induced uterine vasodilation, which is partially cGMP dependent. Systemic vascular KV also contributes to maintaining MAP after systemic E2β.

Oxygen, glucose, and lactate uptake by fetus and placenta during prolonged hypoxemia

1995 ◽  
Vol 268 (2) ◽  
pp. R303-R309 ◽  
Author(s):  
S. B. Hooper ◽  
D. W. Walker ◽  
R. Harding
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Lactate Clearance ◽  
Gravid Uterus ◽  
Uterine Blood Flow ◽  
Fetal Circulation ◽  
Umbilical Blood ◽  
Pregnant Sheep ◽  
Lactate Uptake ◽  
Arterial O2 Saturation

Our aim was to compare the effects of short (4 h) and prolonged (24 h) periods of reduced uterine blood flow (RUBF) on fetal and placental uptake of O2, glucose, and lactate. In pregnant sheep, uterine and umbilical blood flows were measured under normal conditions and after 4 and 24 h of RUBF. A 50% reduction in uterine blood flow caused a 56% reduction in fetal arterial O2 saturation (SaO2). Umbilical blood flow increased from 325 +/- 33 to 378 +/- 32 ml.min-1.kg-1 (P < 0.05) after 4 h but was not different from pre-RUBF values after 24 h. O2 uptake by the gravid uterus was not altered by RUBF, due to an increase (84%) in uterine O2 extraction. Similarly, uteroplacental and fetal O2 consumptions and fetal glucose uptake were not affected by RUBF, whereas uteroplacental glucose uptake was significantly reduced after 4 h (by 42%) and 24 h (by 58%) of RUBF. Fetal lactate uptake was greatly reduced from 78.7 +/- 15.5 to -167 +/- 57 mumol.min-1.kg-1 after 4 h and to -198 +/- 80 mumol.min-1.kg-1 after 24 h of RUBF; negative values indicate placental lactate uptake from the fetal circulation. Thus, although RUBF significantly reduced fetal SaO2, fetal and uteroplacental O2 consumptions did not change. In addition, although fetal glucose uptake was not altered by RUBF, during RUBF the placenta became a major site of lactate clearance from the fetal circulation.

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