Invited editorial on "effect of altitude on uterine artery blood flow during normal pregnancy" and "alterations in uteroplacental blood flow precede hypertension in preeclampsia at high altitude"

1995 ◽  
Vol 79 (1) ◽  
pp. 5-6
Author(s):  
K. E. Clark
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Uterine Artery ◽  
Normal Pregnancy ◽  
Artery Blood Flow ◽  
Uteroplacental Blood Flow

scholarly journals PSII-7 Uterine artery hemodynamics and placentome quantification during maternal nutrient restriction in beef cattle

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 237-237
Author(s):  
Dana Reid ◽  
Caleb O Lemley ◽  
Kalisha Yankey ◽  
Derris Burnett
Keyword(s):  
Blood Flow ◽  
Beef Cattle ◽  
Uterine Artery ◽  
Late Gestation ◽  
Fetal Weight ◽  
Nutrient Restriction ◽  
Artery Blood Flow ◽  
Uteroplacental Blood Flow ◽  
Group 2 ◽  
Group 1

Abstract Proper fetal nutrition via adequate uteroplacental blood flow is critical for maximizing fetal development and reducing mortality. However, our understanding of adaptations during maternal nutrient restriction is incomplete. The purpose of this study was to determine the effect of nutrient restriction during mid to late gestation on utero-placental hemodynamics and placentome morphometrics in gestating beef cattle. Animals (n = 10) were randomly assigned one of 2 treatments: Control (CON; 100% NRC Requirements) vs Restricted Feed (NR; 60% of NRC Requirements) from 140 to 240 days of gestation. Hemodynamic parameters were collected by Doppler ultrasonography 1 week prior to slaughter from the ipsilateral and contralateral uterine arteries, after which, total uterine artery blood flow was calculated. Six animals (n = 3 per treatment) were slaughtered on day 240 of gestation (Group 1) and the remaining 4 animals were slaughtered on 265 ± 15 days (Group 2). Placentome tissues were harvested for weight and number determination. Placentome number decreased (P = 0.01) in nutrient restricted (49 ± 6) versus control (83 ± 6) fed dams. There was an interaction between treatment and group in which ipsilateral diameter increased (P < 0.05) in group 2 NR animals versus group 2 CON animals while there was no difference between NR and CON in group 1. There was no difference (P = 0.30) in total uterine artery blood flow in fetal weight, which averaged 212 ± 37 mL/min*kg in nutrient restricted versus 153 ± 34 mL/min*kg in control fed dams. In summary, these data indicate limited alterations in uterine artery blood flow and fetal weight in nutrient restricted dams during the last half of gestation. The decrease in placentome number with no difference in placentome weight could indicate larger placentomes in nutrient restricted dams were able to compensate for the reduction in total number.

Influence of sleep and myometrial activity on systemic and uteroplacental hemodynamics in pregnant ewes

1995 ◽  
Vol 268 (4) ◽  
pp. H1734-H1739
Author(s):  
J. E. Fewell
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Uterine Artery ◽  
Systemic Arterial Pressure ◽  
Uterine Horn ◽  
Artery Blood Flow ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Quiet Wakefulness ◽  
Uteroplacental Blood Flow

Little is known about the influence of sleep on systemic and uteroplacental hemodynamics during pregnancy. Experiments were therefore carried out on six chronically instrumented pregnant ewes (125–133 days of gestation) to investigate the influence of sleep on systemic and uteroplacental hemodynamics. Because nonlabor myometrial activity influences uteroplacental hemodynamics, we made measurements during quiet wakefulness, quiet sleep, and active sleep in the presence and absence of myometrial activity. Cardiac output, heart rate, and systemic arterial pressure were decreased in active sleep compared with quiet wakefulness; these variables were not significantly altered by myometrial activity. The interaction between sleep and myometrial activity was such that the lowest values of uteroplacental blood flow, as estimated from middle uterine artery blood flow to the pregnant uterine horn and, hence, uteroplacental oxygen delivery occurred during active sleep in the presence of myometrial activity (i.e., decreased approximately 19% compared with quiet wakefulness and the absence of myometrial activity). Further investigation is required to determine the possible fetal consequences of a reduced uteroplacental perfusion in the presence of myometrial activity during sleep.

scholarly journals Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude

2008 ◽  
Vol 295 (3) ◽  
pp. R906-R915 ◽  
Author(s):  
Colleen Glyde Julian ◽  
Henry L. Galan ◽  
Megan J. Wilson ◽  
Wendy DeSilva ◽  
Darleen Cioffi-Ragan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Birth Weight ◽  
High Altitude ◽  
Fetal Growth ◽  
Uterine Artery ◽  
Weight Variation ◽  
Uteroplacental Blood Flow ◽  
Fetal Size ◽  
Nitric Oxide Metabolites

Reduced uteroplacental blood flow is hypothesized to play a key role in altitude-associated fetal growth restriction. It is unknown whether reduced blood flow is a cause or consequence of reduced fetal size. We asked whether determinants of uteroplacental blood flow were altered prior to reduced fetal growth and whether vasoactive and/or angiogenic factors were involved. Women residing at low (LA; 1600 m, n = 18) or high altitude (HA; 3100 m, n = 25) were studied during pregnancy (20, 30, and 36 wk ) and 4 mo postpartum (PP) using Doppler ultrasound. In each study, endothelin (ET-1), nitric oxide metabolites (NO x), soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF) levels were quantified. At HA, birth weights were lower ( P < 0.01) and small-for-gestational age was more common ( P < 0.05) compared with LA. HA was associated with lower uterine artery (UA) diameter ( P < 0.01) and blood flow ( P < 0.05). Altitude did not affect ET-1, sFlt-1 or PlGF; however, ET-1/NO x was greater and NO x lower during pregnancy and PP at HA vs. LA. ET-1/NO x was negatively associated with birth weight (20 wk, P < 0.01; 36 wk, P = 0.05) at LA and HA combined. At HA, UA blood flow (30 wk) was positively associated with birth weight (†). UA blood flow and ET-1/NO x levels accounted for 45% (20 wk) and 32% (30 wk) of birth weight variation at LA and HA combined, primarily attributed to effects at HA. We concluded that elevated ET-1/NO x and altered determinants of uteroplacental blood flow occur prior to altitude-associated reductions in fetal growth, and therefore, they are likely a cause rather than a consequence of smaller fetal size.

scholarly journals P07.04: Uterine artery blood flow volume is reduced in human pregnancies with increase utero-placental downstream impedance

2006 ◽  
Vol 28 (4) ◽  
pp. 569-569
Author(s):  
S. Boito ◽  
S. Rigano ◽  
G. Pennati ◽  
L. Mandia ◽  
A. Padoan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Flow Volume ◽  
Artery Blood Flow ◽  
Blood Flow Volume

scholarly journals Maternal Uterine Vascular Remodeling During Pregnancy

Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala
Keyword(s):  
Extracellular Matrix ◽  
Blood Flow ◽  
Vascular Remodeling ◽  
Normal Pregnancy ◽  
Uterine Blood Flow ◽  
Growth And Remodeling ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Uteroplacental Blood Flow ◽  
Uterine Circulation

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.

scholarly journals Activation of angiotensin type 2 receptor attenuates testosterone-induced hypertension and uterine vascular resistance in pregnant rats

2021 ◽  
Author(s):  
Jay S Mishra ◽  
Sathish Kumar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Vascular Function ◽  
Uterine Artery ◽  
Artery Blood Flow ◽  
Protein Levels ◽  
Angiotensin Type 2 Receptor ◽  
Enos Protein ◽  
Angiotensin Type

Abstract Preeclampsia is a pregnancy-related hypertensive disorder with unclear mechanisms. While hypersensitivity to angiotensin II via vasoconstrictive angiotensin type-1 receptor (AT1R) is observed in preeclampsia, the importance of vasodilatory angiotensin type-2 receptor (AT2R) in the control of vascular dysfunction is less clear. We assessed whether AT1R, AT2R and eNOS expression is altered in placental vessels of preeclamptic women and tested if ex vivo incubation with AT2R agonist Compound 21 (C21; 1 μM) could restore AT1R, AT2R and eNOS balance. Further, using a rat model of gestational hypertension induced by elevated testosterone, we examined whether C21 (1 μg·kg−1·day−1, oral) could preserve AT1R and AT2R balance and improve blood pressure, uterine artery blood flow, and vascular function. Western blots revealed that AT1R protein level was higher while AT2R and eNOS protein were reduced in preeclamptic placental vessels, and AT2R agonist C21 decreased AT1R and increased AT2R and eNOS protein levels in preeclamptic vessels. In testosterone-dams, blood pressure was higher, and uterine artery blood flow was reduced, and C21 treatment reversed these levels similar to those in controls dams. C21 attenuated the exaggerated Ang II contraction and improved endothelium-dependent vasorelaxation in uterine arteries of testosterone-dams. These C21-mediated vascular effects were associated with decreased AT1R and increased AT2R and eNOS protein levels. C21 also increased serum nitrate/nitrite and bradykinin production in testosterone-dams and attenuated the feto-placental growth restriction. Thus, AT1R upregulation and AT2R downregulation is observed in preeclampsia and testosterone-model, and increasing AT2R activity could help restore AT1R and AT2R balance and improve gestational vascular function.

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