Vein size in intact and hysterectomized mice during the estrous cycle and pregnancy

Forbes, Thomas R.; Taku, Elaine

doi:10.1002/ar.1091820107

Cited by 11 publications

(11 citation statements)

References 19 publications

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“…Vessel dimensions in the nonpregnant horn were similar to those of a nonpregnant animal in terms of the length and diameter of both large and small arteries. Consistent with this, uterine vein size was found to be increased only in the pregnant horn of single horn ligated mice, with values from the nonpregnant horn being similar to that of nonpregnant controls (34). …”

Section: Mechanisms Underlying Gestational Uterine Vascular Remodelingsupporting

confidence: 70%

“…Increased venous diameter was also accompanied by increased distensibility and reduced elastin content, adaptations that would further enhance venous capacitance. Significant uterine venous enlargement during pregnancy was also reported in the mouse (34). …”

Section: Pattern Nature and Extent Of Uterine Vascular Remodeling Dmentioning

confidence: 62%

“…The uterine horn ligation model has been used to explore a variety of pregnancy-related questions in several species, including the cow (35), pig (36, 60), rabbit (137), guinea pig (128), rat (136), and mouse (34), and the available evidence points to local rather than systemic factors playing a primary role in gestational uterine vascular remodeling and increases in blood flow.…”

Section: Mechanisms Underlying Gestational Uterine Vascular Remodelingmentioning

confidence: 99%

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Maternal Uterine Vascular Remodeling During Pregnancy

2009

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This classification was proposed by Mulvany (86) and is further refined to include consideration of wall mass, which can increase (hypertrophy), decrease (hypotrophy), or remain unchanged (eutrophy). Various patterns of arterial remodeling are shown in FIGURE 1; see legend for additional detail and for consideration of how changes in crosssectional area, a two-dimensional quantity (e.g., m 2 ), relate to changes in wall mass, a three-dimensional quantity (e.g., m 3 ). Uterine Hemodynamics DuringPregnancy; Blood Flow Patterns and the Importance of Placentation Type Uterine vascular anatomyAn overview of comparative uterine vascular anatomy is presented in FIGURE 2, which describes and illustrates the uterine circulation in humans (FIGURE 2A), rodents (FIGURE 2B), and ungulates, such as sheep and pigs. Please see legend for additional detail.Uterine and placental blood flow during pregnancy Early (1953Early ( -1960 human studies by Assali et al (3, 4) and Metcalfe (78) utilizing the diffusion equilibrium principle (most often nitrous oxide, N 2 O) or electromagnetic flow probes placed directly on the uterine artery reported that total uteroplacental blood flow (UPBF) increases from a baseline value of 20-50 ml/min to 450-800 ml/min in singleton pregnancies, with values in excess of 1 l/min measured in twin pregnancy. Subsequent measurements of uterine artery blood flow with 133 Xe (106), placental metabolic clearance rate techniques (29) The clinical relevance of maternal uterine vascular adaptation during pregnancy is underscored by the fact that its aberrance is associated with several common gestational pathologies, including intrauterine growth restriction, gestational diabetes, and preeclampsia.In addition to the changes in vessel structure, uterine vascular reactivity is also altered during pregnancy, with the general pattern being one of reduced tone and enhanced vasodilation/blunted vasoconstriction (52,72,111,112,118). Space limitations preclude indepth consideration of the ionic and enzymatic mechanisms that underlie reactivity, but it is worth noting that, in vivo, uterine vascular resistance (and, therefore, blood flow) is ultimately determined by the combination of vessel size and reactivity.We also avoid examining the complex angiogenic mechanisms associated with implantation and placentation, other than to consider how hemochorial vs. epitheliochorial placentation influences uterine hemodynamics and vascular remodeling. Although the remodeling of spiral arteries by fetal trophoblast is considered, the main focus of this review is on upstream maternal uterine arteries and veins, since the processes involved in their remodeling have not been reviewed to date. Readers interested in endovascular trophoblast invasion and mechanisms underlying spiral artery remodeling are referred to several reviews on this subject (9, 31, 71, 101). Nomenclature Used to Describe Vascular RemodelingCircumferential remodeling is normally termed inward or outward to denote narrowing vs. widening of the vessel lumen. The ...

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Section: Mechanisms Underlying Gestational Uterine Vascular Remodelingsupporting

confidence: 70%

Section: Pattern Nature and Extent Of Uterine Vascular Remodeling Dmentioning

confidence: 62%

Section: Mechanisms Underlying Gestational Uterine Vascular Remodelingmentioning

confidence: 99%

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Maternal Uterine Vascular Remodeling During Pregnancy

2009

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“…Increased venous diameter was accompanied by significantly increased endothelial and VSMC mitotic indices, increased distensibility and a reduced elastin content – adaptations that would further enhance venous capacitance [20]. Significant uterine venous enlargement during pregnancy was also reported in the mouse [24].…”

Section: Remodelling Of Uterine Veinsmentioning

confidence: 99%

Physiological Remodelling of the Maternal Uterine Circulation during Pregnancy

Mandalà

Osol

2011

Basic Clin Pharma Tox

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Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodelling of the entire maternal uterine vasculature. The main focus of this MiniReview is to provide information on upstream (pre-placental) maternal uterine vascular remodelling that facilitates gestational increases in uterine blood flow. Consideration of the three-dimensional pattern of remodelling (circumferential enlargement versus axial elongation), changes in vessel biomechanical properties, and underlying mechanisms [shear stress, nitric oxide, vascular endothelial growth factor (VEGF) ⁄ placental growth factor (PlGF), the renin-angiotensin system] and pathways (local versus systemic; venoarterial exchange) are provided using the rat as the principal animal model, although findings from other species are incorporated wherever possible to provide a comparative perspective. The process of maternal gestational uterine vascular remodelling involves a number of cellular processes and mechanisms, including trophoblast invasion, hyperplasia and hypertrophy, and changes in extracellular matrix composition. In addition, changes in cellular function, e.g. the secretory and contractile properties of smooth muscle and an up-regulation of endothelial vasodilatory influences may contribute to uteroplacental blood flow increases through changes in tone as well as in structure. Future studies aimed at better understanding the inter-relationship between changes in vessel structure (remodelling) and function (reactivity) would likely generate new mechanistic insights into the fascinating process of maternal gestational uterine vascular adaptation and provide a more physiological perspective of the underlying cellular processes involved in its regulation.

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“…The uterine vasculature undergoes considerable growth and remodeling during pregnancy, a process that leads to significant increases in uterine blood flow characteristic of mammalian gestation [1][2][3][4][5][6]. The purpose of this process is to accommodate the increasing demands of the developing fetus with respect to oxygen and nutrient delivery.…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic, Vascular, and Reproductive Impact of FMS-Like Tyrosine Kinase 1 (FLT1) Blockade on the Uteroplacental Circulation During Normal Mouse Pregnancy1

Khankin

Mandalà

Colton

et al. 2012

Biology of Reproduction

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To investigate the role of FMS-like tyrosine kinase 1 (FLT1, also known as VEGFR1) signaling during pregnancy, mice were injected with anti-FLT1 neutralizing antibody (Ab) beginning on Gestational Day 8 or 12 and every other day thereafter until Day 18; vehicle-only injected mice served as controls. Uterine artery blood flow was measured with ultrasound on Days 13 and 18, and morphometric measurements of the uterine arcade were carried out on Day 19 to provide a measure of gestational vascular remodeling; reproductive performance was evaluated by determining litter size, resorption rates, and pup and placental weights. Ab injections beginning on Day 8 or Day 12 resulted in significant reductions of uterine artery peak systolic and diastolic flows at Days 13 and 18. In addition, normal reproductive function was compromised, as evidenced by a significant reduction in average number of viable pups along with enhanced resorption rates. Reproductive performance was also significantly compromised in this group, although less severely. There was no evidence of a reduction in main uterine artery diameters, though arterial distensibility was reduced, and the diameter of the main uterine vein was significantly smaller in the Ab-injected mice. Significant reductions in main uterine artery and segmental artery length were also noted. Placental and pup weights were similar in all the groups. FLT1 inhibition during murine pregnancy impaired blood flow to the fetalplacental unit, compromised several indices of vascular remodeling, reduced fecundity, and increased fetal reabsorptions. The effects of FLT1 inhibition are most pronounced when targeted during early pregnancy.angiogenesis, FLT1, pregnancy, sFLT1, ultrasound, uterine artery, uterine vein, vascular remodeling, VEGF

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Vein size in intact and hysterectomized mice during the estrous cycle and pregnancy

Cited by 11 publications

References 19 publications

Maternal Uterine Vascular Remodeling During Pregnancy

Maternal Uterine Vascular Remodeling During Pregnancy

Physiological Remodelling of the Maternal Uterine Circulation during Pregnancy

Hemodynamic, Vascular, and Reproductive Impact of FMS-Like Tyrosine Kinase 1 (FLT1) Blockade on the Uteroplacental Circulation During Normal Mouse Pregnancy1

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