scholarly journals Uteroplacental Circulation in Normal Pregnancy and Preeclampsia: Functional Adaptation and Maladaptation

2021 ◽  
Vol 22 (16) ◽  
pp. 8622
Author(s):  
Xiangqun Hu ◽  
Lubo Zhang
Keyword(s):  
Blood Flow ◽  
Hormonal Regulation ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Well Being ◽  
Normal Pregnancy ◽  
Functional Adaptation ◽  
Vasoactive Factors ◽  
Uteroplacental Blood Flow ◽  
Underlying Mechanisms

Uteroplacental blood flow increases as pregnancy advances. Adequate supply of nutrients and oxygen carried by uteroplacental blood flow is essential for the well-being of the mother and growth/development of the fetus. The uteroplacental hemodynamic change is accomplished primarily through uterine vascular adaptation, involving hormonal regulation of myogenic tone, vasoreactivity, release of vasoactive factors and others, in addition to the remodeling of spiral arteries. In preeclampsia, hormonal and angiogenic imbalance, proinflammatory cytokines and autoantibodies cause dysfunction of both endothelium and vascular smooth muscle cells of the uteroplacental vasculature. Consequently, the vascular dysfunction leads to increased vascular resistance and reduced blood flow in the uteroplacental circulation. In this article, the (mal)adaptation of uteroplacental vascular function in normal pregnancy and preeclampsia and underlying mechanisms are reviewed.

scholarly journals Residual vascular dysfunction in women with a history of preeclampsia

2018 ◽  
Vol 315 (6) ◽  
pp. R1062-R1071 ◽  
Author(s):  
Anna E. Stanhewicz
Keyword(s):  
Vascular Function ◽  
Vascular Dysfunction ◽  
Normal Pregnancy ◽  
The United States ◽  
Hypertensive Disorder ◽  
Vascular Endothelial ◽  
Cvd Risk ◽  
History Of ◽  
Hypertensive Disorder Of Pregnancy ◽  
Underlying Mechanisms

Preeclampsia is a hypertensive disorder of pregnancy characterized by new-onset hypertension, proteinuria, and edema occurring after 20 wk of gestation, with a prevalence of ~7–10% of pregnancies in the United States and ~8 million pregnancies worldwide. Despite the postpartum remission of preeclamptic symptoms, women who have had preeclampsia are two to four times more likely to develop cardiovascular disease (CVD) and are significantly more likely to die of CVD compared with women with a history of normal pregnancy. Although the relation between history of preeclampsia and elevated CVD risk is well documented, the mechanism(s) underlying this association remains unclear. One hypothesis explaining this association is that the initial vascular damage and dysfunction sustained during the preeclamptic pregnancy persist chronically. Indeed, even in the absence of, or in advance of, overt CVD women who have had preeclampsia have compromised vascular endothelial function. Emerging mechanistic studies in these women have provided some insight into the underlying mechanisms of this persistent vascular dysfunction and have begun to identify potential therapeutic targets for the prevention or mitigation of CVD progression in this vulnerable population. This review summarizes the existing literature examining vascular function and dysfunction in women with a history of preeclampsia and highlights future directions for mechanistic investigations and development of novel intervention strategies aimed at halting or slowing the progression of CVD in these women.

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.

Abstract 14820: Sirt7 Deficiency in Blood Vessel Components Impairs Vascular Function by Inhibiting Cell Cycle- and Inflammatory-Related Protein Expression

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yuichi Kimura ◽  
Yasuhiro Izumiya ◽  
Satoshi Araki ◽  
Satoru Yamamura ◽  
Yoshiro Onoue ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Vascular Diseases ◽  
Tube Formation ◽  
Hindlimb Ischemia ◽  
Proliferation Assay

Introduction: Aging is a well-established cardiovascular risk factor and associated with vascular dysfunction. Sirt7, one of the members of mammalian sirtuin family, is thought to be involved in age-related diseases. However, little is known about the relative contribution of Sirt7 in vascular dysfunction. Hypothesis: Sirt7 maintains vascular cell functions and its deficiency plays a critical role in vascular diseases. Methods: Sirt7 loss- and gain-of-function experiments were performed with human aortic smooth muscle cells (HAoSMCs) and human umbilical vein endothelial cells (HUVECs). In vivo, blood flow recovery was evaluated by hindlimb ischemia model in homozygous Sirt7 deficient (Sirt7-/-) and wild-type (WT) mice. Irradiated WT mice were intravenously received bone marrow (BM) cells from WT or Sirt7 -/- mouse to achieve BM transfer. Results: An RNAi-medicated Sirt7 knockdown resulted in a significant inhibition of HAoSMCs proliferation following serum or Platelet-derived growth factor BB (PDGF-BB) stimulation as determined by cell count, BrdU cell proliferation assay and MTS proliferation assay. Knockdown of endogenous Sirt7 also reduced cell migration as revealed by Boyden chamber migration assay. The Cyclin D1 and Cyclin dependent kinase 2 (CDK2) protein levels were significantly decreased in Sirt7 siRNA-treated HAoSMCs in response to serum or PDGF-BB stimulation. In endothelial cells, knockdown of Sirt7 attenuated tube formation, proliferation and migration. These changes were accompanied by reduced ERK activation and VCAM-1 mRNA and protein expression in Sirt7 siRNA-treated HUVECs. Conversely, overexpression of Sirt7 by adenovirus enhanced tube formation and cell proliferation. In vivo, blood flow recovery in response to hindlimb ischemia was significantly attenuated in Sirt7-/- mice compared with WT mice. There was no difference in blood flow recovery between WT mice transplanted with WT or Sirt7-/- BM cells suggesting that Sirt7 deficiency in vascular cells have a predominant effect on attenuated blood flow recovery in response to hindlimb ischemia. Conclusions: Sirt7 in blood vessel components have an important role in maintenance of vascular function. Sirt7 could be a promising therapeutic target for vascular diseases.

scholarly journals Delineating the age-related attenuation of vascular function: Evidence supporting the efficacy of the single passive leg movement as a screening tool

2019 ◽  
Vol 126 (6) ◽  
pp. 1525-1532 ◽  
Author(s):  
Jay R. Hydren ◽  
Ryan M. Broxterman ◽  
Joel D. Trinity ◽  
Jayson R. Gifford ◽  
Oh Sung Kwon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Function ◽  
Screening Test ◽  
Vascular Dysfunction ◽  
Peripheral Vascular ◽  
Leg Blood Flow ◽  
Age Related ◽  
Cut Score ◽  
Leg Movement ◽  
Hyperemic Response

Continuous passive leg movement (PLM) is a promising clinical assessment of the age-related decline in peripheral vascular function. To further refine PLM, this study evaluated the efficacy of a single PLM (sPLM), a simplified variant of the more established continuous movement approach, to delineate between healthy young and old men based on vascular function. Twelve young (26 ± 5 yr) and 12 old (70 ± 7 yr) subjects underwent sPLM (a single passive flexion and extension of the knee joint through 90°), with leg blood flow (LBF, common femoral artery with Doppler ultrasound), blood pressure (finger photoplethysmography), and leg vascular conductance (LVC) assessed. A receiver operator characteristic curve analysis was used to determine an age-specific cut score, and a factor analysis was performed to assess covariance. Baseline LBF and LVC were not different between groups ( P = 0.6). The high level of covariance and similar predictive value for all PLM-induced LBF and LVC responses indicates LBF, alone, can act as a surrogate variable in this paradigm. The peak sPLM-induced increase in LBF from baseline was attenuated in the old (Young: 717 ± 227, Old: 260 ± 97 ml/min, P < 0.001; cut score: 372 ml/min), as was the total LBF response (Young: 155 ± 67, Old: 26 ± 17 ml, P < 0.001; cut score: 58 ml). sPLM, a simplified version of PLM, exhibits the prerequisite qualities of a valid screening test for peripheral vascular dysfunction, as evidenced by an age-related attenuation in the peripheral hyperemic response and a clearly delineated age-specific cut score. NEW & NOTEWORTHY Single passive leg movement (sPLM) exhibits the prerequisite qualities of a valid screening test for peripheral vascular dysfunction. sPLM displayed an age-related reduction in the peripheral hemodynamic response for amplitude, duration, initial rate of change, and total change with clearly delineated age-specific cut scores. sPLM has a strong candidate variable that is a simple single numeric value, for which to appraise peripheral vascular function, the 45-s hyperemic response (leg blood flow area under the curve: 45 s).

scholarly journals Algorithm of echocardiography in pregnant women

2018 ◽  
pp. 75-83
Author(s):  
S. G. Gorokhova ◽  
T. E. Morozova ◽  
A. A. Arakelyants ◽  
E. A. Barabanova ◽  
E. G. Dyakonova
Keyword(s):  
Blood Flow ◽  
Pregnant Woman ◽  
Physiological Condition ◽  
Heart Diseases ◽  
Healthy Woman ◽  
Normal Pregnancy ◽  
Functional Adaptation ◽  
Pathological Changes ◽  
Placental Blood ◽  
Placental Blood Flow

Pregnancy is a physiological condition that takes a defined period of time in a woman’s life. For nine months, the mother’s heart works under conditions of daily additional load, which is necessary to ensure placental blood flow. In this regard, structural and functional adaptation of the heart develops in a healthy woman with a normal pregnancy. A pregnant woman with some heart diseases is less likely to adapt. That leads to greater susceptibility to stress resulting in pathological changes of pregnancy. In addition, each pregnancy may develop new heart diseases, which in some cases may be relatively innocent, but in others — fatal. In this regard echocardiography (EchoCG) is a necessary procedure for assessing a woman’s health status that needs before bearing a fetus, during and after pregnancy.

scholarly journals Diabetes and the maternal resistance vasculature

2001 ◽  
Vol 101 (6) ◽  
pp. 719-729 ◽  
Author(s):  
Christine ANG ◽  
Mary Ann LUMSDEN
Keyword(s):  
Blood Flow ◽  
Vascular Endothelium ◽  
Pregnancy Outcomes ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Tissue Perfusion ◽  
Endocrine Disorder ◽  
Patient Morbidity ◽  
Adverse Pregnancy

Diabetes is the most common endocrine disorder worldwide, with complications that include the development of both macro- and micro-vascular disease that contribute significantly to patient morbidity and mortality. The severity of diabetic complications is amplified during pregnancy, resulting in a higher incidence of adverse pregnancy outcomes such as pre-eclampsia, placental insufficiency and stillbirth than in non-diabetics. Vascular dysfunction is thought to underlie many of these complications, with the greatest impact occurring at the level of the resistance vasculature, where alterations in vascular reactivity can significantly affect blood flow and tissue perfusion. It is likely that problems associated with diabetic pregnancies are related, in part, to abnormal vascular function, particularly dysfunction of the vascular endothelium.

Methylation-reprogrammed CHRM3 results in vascular dysfunction in the human umbilical vein following IVF-ET

2021 ◽  
Author(s):  
Yajun Shi ◽  
Jingliu Liu ◽  
Dan Zhu ◽  
Likui Lu ◽  
Mengshu Zhang ◽  
...  
Keyword(s):  
Vascular Function ◽  
Vascular Dysfunction ◽  
Umbilical Vein ◽  
Plasma Lipid ◽  
Normal Pregnancy ◽  
Receptor Subtype ◽  
Functional Studies ◽  
Long Run ◽  
Mlc20 Phosphorylation ◽  
Ivf Et

Abstract Assisted reproductive technology (ART) has been used globally among infertile couples. However, many epidemiological investigations have indicated that ART is associated with a range of long-term adverse health outcomes in offspring, including cardiovascular disease, obesity and increased plasma lipid levels. Until now, direct evidence has been limited regarding the pathological changes in vascular function in fetuses with ART. In this study, human umbilical cords were collected from healthy normal pregnancies and IVF-ET pregnancies. Vascular functional studies involving acetylcholine (ACh), antagonists of its specific receptors, and L-type calcium channel/PKC-MLC20 phosphorylation pathway specific inhibitors were conducted. Quantitative real-time PCR, Western blotting and methylation analyses were performed on umbilical vein samples. We found that the umbilical vein constriction induced by ACh in the IVF-ET group was significantly attenuated compared with that in the healthy normal pregnancy group, which was not only associated with the hypermethylation of ACh muscarinic receptor subtype 3 (CHRM3) and decreased expression of CHRM3, PKCβ and CaV1.2, but was also related to the reduced phosphorylation of MLC20. The present study revealed that the hypermethylation of CHRM3, leading to a reduction in CHRM3 expression and downregulation of the CaV1.2/PKC-MLC20 phosphorylation pathway, was responsible for the decreased sensitivity to ACh observed in the umbilical vein under IVF-ET conditions. The hypermethylation of CHRM3 caused by IVF-ET might play an important role in altered vasoconstriction and impact cardiovascular systems in the long run.

scholarly journals Exercise-induced brachial artery blood flow and vascular function is impaired in systemic sclerosis

2016 ◽  
Vol 311 (6) ◽  
pp. H1375-H1381 ◽  
Author(s):  
Daniel R. Machin ◽  
Heather L. Clifton ◽  
Ryan S. Garten ◽  
Jayson R. Gifford ◽  
Russell S. Richardson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Systemic Sclerosis ◽  
Brachial Artery ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Artery Blood Flow ◽  
Handgrip Exercise ◽  
Brachial Artery Diameter ◽  
Exercise Induced

Systemic sclerosis (SSc) is a rare autoimmune disease characterized by debilitating fibrosis and vascular dysfunction; however, little is known about the circulatory response to exercise in this population. Therefore, we examined the peripheral hemodynamic and vasodilatory responses to handgrip exercise in 10 patients with SSc (61 ± 4 yr) and 15 age-matched healthy controls (56 ± 5 yr). Brachial artery diameter, blood flow, and mean arterial pressure (MAP) were determined at rest and during progressive static-intermittent handgrip exercise. Patients with SSc and controls were similar in body stature, handgrip strength, and MAP; however, brachial artery blood flow at rest was nearly twofold lower in patients with SSc compared with controls (22 ± 4 vs. 42 ± 5 ml/min, respectively; P < 0.05). Additionally, SSc patients had an ∼18% smaller brachial artery lumen diameter with an ∼28% thicker arterial wall at rest ( P < 0.05). Although, during handgrip exercise, there were no differences in MAP between the groups, exercise-induced hyperemia and therefore vascular conductance were ∼35% lower at all exercise workloads in patients with SSc ( P < 0.05). Brachial artery vasodilation, as assessed by the relationship between Δbrachial artery diameter and Δshear rate, was significantly attenuated in the patients with SSc ( P < 0.05). Finally, vascular dysfunction in the patients with SSc was accompanied by elevated blood markers of oxidative stress and attenuated endogenous antioxidant activity ( P < 0.05). Together, these findings reveal attenuated exercise-induced brachial artery blood flow and conduit arterial vasodilatory dysfunction during handgrip exercise in SSc and suggest that elevated oxidative stress may play a role.

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