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Relevant bibliographies by topics / Fetal heart development

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Academic literature on the topic 'Fetal heart development'

Author: Grafiati

Published: 9 March 2023

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Journal articles on the topic "Fetal heart development"

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J. Patterson, A., and L. Zhang. "Hypoxia and Fetal Heart Development." Current Molecular Medicine 10, no. 7 (October 1, 2010): 653–66. http://dx.doi.org/10.2174/156652410792630643.

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Bae, Soochan, Yuhui Xiao, Guohu Li, Carlos A. Casiano, and Lubo Zhang. "Effect of maternal chronic hypoxic exposure during gestation on apoptosis in fetal rat heart." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H983—H990. http://dx.doi.org/10.1152/ajpheart.00005.2003.

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Chronic hypoxia during pregnancy is one of the most common insults to fetal development. We tested the hypothesis that maternal hypoxia induced apoptosis in the hearts of near-term fetal rats. Pregnant rats were divided into two groups, normoxic control and continuous hypoxic exposure (10.5% O2) from day 15 to 21 of gestation. Hearts were isolated from fetal rats of 21-day gestational age. Maternal hypoxia increased hypoxia-inducible factor-1α protein in fetal hearts. Chronic hypoxia significantly increased the percentage and size of binucleated myocytes and increased apoptotic cells from 1.4 ± 0.14% to 2.7 ± 0.3% in the fetal heart. In addition, the active cleaved form of caspase 3 was significantly increased in the hypoxic heart, which was associated with an increase in caspase 3 activity. There was a significant increase in Fas protein levels in the hypoxic heart. Chronic hypoxia did not change Bax protein levels but significantly decreased Bcl-2 proteins. In addition, chronic hypoxia significantly suppressed expression of heat shock protein 70. However, chronic hypoxia significantly increased expression of the anti-apoptotic protein 14–3-3 θ, among other 14–3-3 isoforms. Chronic hypoxia differentially regulated β-adrenoreceptor (β-AR) subtypes with an increase in β1-AR levels but no changes in β2-AR. The results demonstrate that maternal hypoxia increases apoptosis in fetal rat heart, which may be mediated by an increase in Fas and a decrease in Bcl-2 proteins. Chronic hypoxia-mediated increase in β1-AR and decrease in heat shock proteins may also play an important role in apoptosis in the fetal heart.

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Morrison, J. L., K. J. Botting, J. L. Dyer, S. J. Williams, K. L. Thornburg, and I. C. McMillen. "Restriction of placental function alters heart development in the sheep fetus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 1 (July 2007): R306—R313. http://dx.doi.org/10.1152/ajpregu.00798.2006.

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Placental insufficiency, resulting in restriction of fetal substrate supply, is a major cause of intrauterine growth restriction (IUGR) and increased neonatal morbidity. Fetal adaptations to placental restriction maintain the growth of key organs, including the heart, but the impact of these adaptations on individual cardiomyocytes is unknown. Placental and hence fetal growth restriction was induced in fetal sheep by removing the majority of caruncles in the ewe before mating (placental restriction, PR). Vascular surgery was performed on 13 control and 11 PR fetuses at 110–125 days of gestation (term: 150 ± 3 days). PR fetuses with a mean gestational Po2 < 17 mmHg were defined as hypoxic. At postmortem (<135 or >135 days), fetal hearts were collected, and cardiomyocytes were isolated and fixed. Proliferating cardiomyocytes were counted by immunohistochemistry of Ki67 protein. Cardiomyocytes were stained with methylene blue to visualize the nuclei, and the proportion of mononucleated cells and length and width of cardiomyocytes were measured. PR resulted in chronic fetal hypoxia, IUGR, and elevated plasma cortisol concentrations. Although there was no difference in relative heart weights between control and PR fetuses, there was an increase in the proportion of mononucleated cardiomyocytes in PR fetuses. Whereas mononucleated and binucleated cardiomyocytes were smaller, the relative size of cardiomyocytes when expressed relative to heart weight was larger in PR compared with control fetuses. The increase in the relative proportion of mononucleated cardiomyocytes and the relative sparing of the growth of individual cardiomyocytes in the growth-restricted fetus are adaptations that may have long-term consequences for heart development in postnatal life.

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Arai, Masashi. "Antenatal Glucocorticoid Therapy for Fetal Heart Development." Circulation Journal 74, no. 1 (2010): 47–48. http://dx.doi.org/10.1253/circj.cj-09-0827.

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Strizhakov, A. N., A. M. Rodionova, I. V. Ignatko, and V. A. Zaidenov. "Effect of infection on the development of fetal arrhythmias." Voprosy ginekologii, akušerstva i perinatologii 21, no. 3 (2022): 6–12. http://dx.doi.org/10.20953/1726-1678-2022-3-6-12.

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Objective. To assess the impact of infection on the development of fetal arrhythmias. Patients and methods. The study included 84 pregnant women who were divided into two groups: the study group, which consisted of 44 patients aged 20–42 years (Me 31 ± 0.93 years) with fetal arrhythmia and/or minor heart defects at 21–41 weeks’ gestation (Me 37.41 ± 0.58 weeks), and the comparison group, which enrolled 40 pregnant women without fetal heart defects and with normal fetal heart rate to determine the significance of serological markers of myocarditis. Results. Significant titers of non-specific anti-myocardial antibodies to vascular smooth muscle and endothelium were detected in 14 (31.8%) and 7 (15.9%) fetuses, respectively. “Conditionally positive” titers for anti-smooth muscle antibodies were detected in 3 (6.8%) fetuses and for anti-endothelial cell antibodies in 4 (9%) fetuses. There was no significant increase in specific anti-heart antibody titers in both groups. Conclusion. Hypoxia should be considered as a trigger for fetal arrhythmias. The infectious and inflammatory processes are one of the links in the pathogenesis of fetal arrhythmias. Key words: fetal arrhythmia, intrauterine infection, minor heart defects

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Hofman, Paul L., Kelly Hiatt, Mervin C. Yoder, and Scott A. Rivkees. "A1 adenosine receptors potently regulate heart rate in mammalian embryos." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 4 (October 1, 1997): R1374—R1380. http://dx.doi.org/10.1152/ajpregu.1997.273.4.r1374.

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A1adenosine receptors (A1ARs) have been recently shown to be expressed in rodent embryonic hearts at very early stages of development. To determine the functional significance of fetal cardiac A1AR expression during embryogenesis, murine fetal heart preparations were studied between postconceptual days 9 and 12. Dose-response curves generated using a variety of adenosine agonists revealed that A1AR activation potently regulated fetal heart rates. The A1AR agonist, N 6-cyclopentyladenosine, inhibited heart rates in a dose-dependent manner (half-maximal effective concentration = 3.6 × 10−8 M) and stopped fetal cardiac contractions in 63% of preparations. In contrast, A2a and A2b receptor activation did not alter heart rates, and activation of A3 receptors produced modest declines in heart rates. Endogenous adenosine also acted tonically to suppress fetal heart rates, as demonstrated by the A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine, increasing heart rates, whereas the adenosine reuptake blocker dipyridamole lowered fetal heart rates. Pertussis toxin treatment blocked A1AR action, showing that A1AR action was G protein mediated. Using drugs that alter cAMP levels and ion channel action, we were able to show that A1AR action involves events mediated by cAMP, ATP-dependent K, L-type calcium, sodium, and chloride channels, and the pacemaker current. These data show that adenosine and A1ARs potently regulate mammalian heart rates via multiple effector systems at very early stages of prenatal development.

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Antipatis, Christos, Cheryl J. Ashworth, George Grant, Richard G. Lea, Susan M. Hay, and William D. Rees. "Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 6 (December 1, 1998): L1184—L1191. http://dx.doi.org/10.1152/ajplung.1998.275.6.l1184.

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Vitamin A is required during pregnancy for fetal lung development. These experiments monitored fetal lung morphology in normal and vitamin A-deficient rats. The expression of elastin and the growth arrest-specific gene 6 ( gas6) in fetal and neonatal hearts and lungs was assessed by Northern blotting. In normal-fed rats, elastin and gas6 were expressed in the fetal lung and heart from day 19 of gestation up to day 2 postnatally. Maternal vitamin A deficiency altered fetal lung development. On day 20, the bronchial passageways were less developed and showed reduced staining for elastic fibers, and in the neonates, the relative air space and the size of the sacculi were reduced. In the fetal lung, the mRNAs for elastin and gas6 were reduced to 56 and 68% of the control values, respectively. In the fetal heart, the mRNA for elastin was reduced to 64% of the control value, whereas gas6 was increased twofold. In the neonate, there was no change in elastin expression in the lung or heart, but gas6 expression in the heart was increased twofold. These results suggest that, in the pregnant rat, vitamin A deficiency may retard fetal lung development or influence the differentiation of critical cell lines. The changes in elastin and gas6 expression may be used to identify the cell types affected.

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Salman, Huseyin Enes, and Huseyin Cagatay Yalcin. "Computational Modeling of Blood Flow Hemodynamics for Biomechanical Investigation of Cardiac Development and Disease." Journal of Cardiovascular Development and Disease 8, no. 2 (January 31, 2021): 14. http://dx.doi.org/10.3390/jcdd8020014.

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The heart is the first functional organ in a developing embryo. Cardiac development continues throughout developmental stages while the heart goes through a serious of drastic morphological changes. Previous animal experiments as well as clinical observations showed that disturbed hemodynamics interfere with the development of the heart and leads to the formation of a variety of defects in heart valves, heart chambers, and blood vessels, suggesting that hemodynamics is a governing factor for cardiogenesis, and disturbed hemodynamics is an important source of congenital heart defects. Therefore, there is an interest to image and quantify the flowing blood through a developing heart. Flow measurement in embryonic fetal heart can be performed using advanced techniques such as magnetic resonance imaging (MRI) or echocardiography. Computational fluid dynamics (CFD) modeling is another approach especially useful when the other imaging modalities are not available and in-depth flow assessment is needed. The approach is based on numerically solving relevant physical equations to approximate the flow hemodynamics and tissue behavior. This approach is becoming widely adapted to simulate cardiac flows during the embryonic development. While there are few studies for human fetal cardiac flows, many groups used zebrafish and chicken embryos as useful models for elucidating normal and diseased cardiogenesis. In this paper, we explain the major steps to generate CFD models for simulating cardiac hemodynamics in vivo and summarize the latest findings on chicken and zebrafish embryos as well as human fetal hearts.

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Hahurij, Nathan D., Emmeline E. Calkoen, Monique R. M. Jongbloed, Arno A. W. Roest, Adriana C. Gittenberger-de Groot, Robert E. Poelmann, Marco C. De Ruiter, Conny J. van Munsteren, Paul Steendijk, and Nico A. Blom. "Echocardiographic Assessment of Embryonic and Fetal Mouse Heart Development: A Focus on Haemodynamics and Morphology." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/531324.

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Background. Heart development is a complex process, and abnormal development may result in congenital heart disease (CHD). Currently, studies on animal models mainly focus on cardiac morphology and the availability of hemodynamic data, especially of the right heart half, is limited. Here we aimed to assess the morphological and hemodynamic parameters of normal developing mouse embryos/fetuses by using a high-frequency ultrasound system.Methods. A timed breeding program was initiated with a WT mouse line (Swiss/129Sv background). All recordings were performed transabdominally, in isoflurane sedated pregnant mice, in hearts of sequential developmental stages: 12.5, 14.5, and 17.5 days after conception (n=105).Results. Along development the heart rate increased significantly from 125 ± 9.5 to 219 ± 8.3 beats per minute. Reliable flow measurements could be performed across the developing mitral and tricuspid valves and outflow tract. M-mode measurements could be obtained of all cardiac compartments. An overall increase of cardiac systolic and diastolic function with embryonic/fetal development was observed.Conclusion. High-frequency echocardiography is a promising and useful imaging modality for structural and hemodynamic analysis of embryonic/fetal mouse hearts.

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DiPietro, Janet A., Denice M. Hodgson, Kathleen A. Costigan, Sterling C. Hilton, and Timothy R. B. Johnson. "Development of fetal movement — fetal heart rate coupling from 20 weeks through term." Early Human Development 44, no. 2 (February 1996): 139–51. http://dx.doi.org/10.1016/0378-3782(95)01704-6.

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Dissertations / Theses on the topic "Fetal heart development"

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Ali, Mohd Alauddin Mohd. "Development of a portable fetal and maternal heart recorder." Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239928.

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Rog-Zielinska, Eva Alicia. "Role of glucocorticoid signalling in fetal heart development and maturation." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8086.

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Glucocorticoids are steroid hormones that affect a variety of physiological and pathological processes both throughout development and in adult life. During mammalian fetal growth, the late gestation rise in fetal glucocorticoid levels is essential for the maturation of tissues and organs in preparation for birth. In humans, glucocorticoids are routinely administered to women threatened by a preterm labour to accelerate fetal lung maturation and prevent neonatal respiratory distress and mice lacking glucocorticoid receptor (GR-/- mice) die neonatally as they are unable to inflate their lungs due to severe pulmonary immaturity. Apart from their importance for proper lung maturation, the physiological role of glucocorticoids in the development of other organs and tissues is not well known. However, prenatal exposure to excess glucocorticoids was shown to elicit detrimental “programming” effects, raising the susceptibility to adult diseases such as hypertension, obesity and metabolic disturbances in both humans and animal models. I therefore used global and conditional GR knock out mouse models to investigate the role and importance of adequate glucocorticoid signalling in fetal heart development and maturation. I further confirmed the direct effects of glucocorticoids on the cardiomyocyte structure and function in an in vitro setting. GR-/- fetuses are under-represented in late gestation (>50% of the number of GR+/+ littermates) but are present in the expected mendelian ratio at E14.5. At E17.5, GR-/- fetuses show edema (increased fluid accumulation and body sodium content). Excess extracellular fluid accumulation could be a result of a congenital heart failure. During development, corticosterone levels sharply increase within the fetal hearts at E15.5-E16.5, coincident with nuclear translocation of GR. Consistent with activation of GR only after this time, the phenotypic consequences of GR deficiency can be seen after E16.5 and not before. At E17.5, hearts of GR-/- fetuses are smaller than in GR+/+ but display no structural abnormalities. Cardiac function however is severely impaired, with left ventricular systolic and diastolic performance inferior in GR-/- fetuses compared to their wild-type littermates. Microscopically, at E17.5, the structure of the cardiac muscle and individual cardiomyocytes are affected by the lack of GR. The normal outer muscle layer, with characteristic rod-shaped, aligned cardiomyocytes is not discernable in the GR-/- heart. Within the cardiomyocytes, myofibrils are short, undefined and randomly scattered within the cell. Lack of the maturational progression in the GR-/- hearts at E17.5 is evident in the pattern of gene expression. GR-/- fetuses do not display the normal gestational changes between E14.5 and E17.5 that are seen in control mice, including in genes involved in the maturation of cardiac structure (eg myosin heavy chain-α, MyHC-α), function (atrial natriuretic peptide, ANP), energy metabolism (eg hexokinase-1, PPARγ coactivator-1α, PGC-1α) and calcium handling (ryanodine receptor, RyR; sarcoplasmic reticulum Ca2+-ATPase, SERCA2a). However, there are no genotype or gestational alterations in mRNA encoding the mineralocorticoid receptor, which is also a receptor for glucocorticoids in the heart. The normal gestational changes in the levels of modified histone H3 associated with the promoters of some of the genes (MyHC-α, ANP, PGC-1α) are not seen in hearts of GR-/- fetuses. This cardiac phenotype was not secondary to adrenal catecholamine insufficiency reported in other GR-/- models, as peripheral tissue levels of adrenaline were not different between genotypes. In order to test the hypothesis that the effects of glucocorticoids on the heart are mediated via GR in cardiomyocytes and to further elucidate the direct effects of GR deficiency specifically within the heart, mice with conditional deletion of GR selectively in cardiac and vascular smooth muscle cells were generated ("SMGRKO" mice). These show ~65% reduction in cardiac GR mRNA and protein levels. Circulating levels of corticosterone do not differ between genotypes at E17.5. SMGRKO fetuses at E17.5 display a phenotype strikingly similar to that of global GR-/-, namely edema, impaired cardiac function, impaired cellular architecture within the ventricle and alterations in the gene expression, implying that the GR-deficient phenotype is largely due to the direct actions of GR within the heart and not secondary to effects on other systems (eg kidney or liver). In order to investigate the pathways by which GR stimulates cardiomyocyte maturation, an in vitro model of murine primary fetal (E15.5-E16.5) cardiomyocytes was developed. Cultures contain >98% of troponin Tpositive cells which beat spontaneously. Treatment of cardiomyocytes with either synthetic (dexamethasone) or physiological (corticosterone) glucocorticoid induces time- and dose-dependent changes in gene expression, consistent with glucocorticoid-dependent changes seen in vivo in the late gestation heart. The effects of glucocorticoids on gene expression were abolished by either siRNA mediated knock-down of GR or RU486 antagonism of GR, but were unaffected by a mineralocorticoid receptor (MR) antagonist. Moreover, cycloheximide pretreatment (to block protein synthesis) suggested PGC-1α as a direct genomic target of GR. RNAseq transcriptome analysis performed on cardiomyocytes treated with dexamethasone and cycloheximide for 2h identified >600 genes as possible rapid and direct glucocorticoid response targets. Among them are genes involved in energy metabolism, calcium handling and sarcomere assembly. Glucocorticoid treatment of fetal cardiomyocytes also induces striking structural changes – formation of stress troponin T-associated actin fibers and sarcomere assembly. Spontaneous contractile activity is improved by glucocorticoid treatment, with a decrease in both contraction and relaxation time (without a change in frequency) and an improvement in the relaxation kinetics. In summary, glucocorticoid signalling in cardiomyocytes is required for the functional, structural and transcriptional maturation of the fetal heart in late gestation in vivo. Glucocorticoid treatment of primary murine fetal cardiomyocytes replicated the contractile, transcriptional and structural changes seen in vivo and was dependent on GR. Thus, GR is essential in cardiomyocytes for the structural and biochemical changes that underlie the maturation of heart function around the time of birth and an inadequate glucocorticoid environment could potentially lead to detrimental and permanent changes in postnatal cardiac function. Since prenatal glucocorticoids are routinely used clinically, it is important to consider any possible effects they might have on the heart development and its function later in life.

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Cutri, Natalie. "The impact of chronic hypoxia on cardiomyocyte development in the fetal sheep heart /." Title page and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09SB/09sbc9898.pdf.

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Alonge, S. "ULTRASONOGRAPHIC FEATURES OF CANINE PREGNANCY WITH SPECIAL REFERENCE TO FETAL DEVELOPMENT AND HEALTH." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/367050.

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Nowadays ultrasonography represents the gold standard method for the evaluation of canine fetal development and health. In dogs, the gestational age is estimated by the ultrasonographic measurements of extra-fetal and fetal structures. The fetal development has been deeply investigated in small and medium dogs, whereas only few information are available for large and giant size bitches, even though they are very popular canine breeds. The measurements of the inner chorionic cavity (ICC) in early pregnancy, and the biparietal diameter (BP) in late pregnancy are commonly used in clinical practice. Both ICC and BP are highly reliable when size-related specific formulae are applied, thus, specific equations for large and giant dogs would allow the most accurate prediction of parturition term. Only few parameters are available to objectively assess the fetal health during canine pregnancy. Among them, the fetal heart rate (FHR) is generally used, but the relationship between FHR and maternal heart rate (MHR) has been poorly investigated. The availability of reference values of the ratio FHR/MHR, could better contribute to the evaluation of the fetal health at different gestational ages, than the single FHR values. The aims of this study were 1) to derive the growth curves of extra-fetal and fetal structures (ICC and BP) in large and giant size bitches and to evaluate their accuracy (Paper 1); 2) to evaluate the trend of FHR and of the ratio FHR/MHR in bitches of different pre-gestational bodyweight (Paper 2). Present results showed a significant relationship between days before parturition and ICC or BP in large and giant size bitches. The overall accuracy ±2 days of both parameters was significantly higher than the accuracy ±1 day. Only in giant bitches, the BP accuracy of the prediction was significantly lower in small than normal litter size. As previously observed in other sizes dogs, the gender did not affect the accuracy of the prediction. The second study demonstrated that both FHR and FHR/MHR significantly fitted a multiple quadratic regression for all independent variables. They both resulted higher in low and high bodyweight, and reached the maximum values at about 20 days before parturition. Maternal pre-gestational bodyweight and the gestational age influenced both FHR and FHR/MHR. The highest significance of FHR/MHR, compared to FHR, encourages the application of this ratio, to evaluate fetal health. The derived equation for FHR/MHR ratio, that describes the trend in healthy fetuses, could be helpful in clinical practice to derive expected values in uncomplicated pregnancies.

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McKean, Josephine Kay. "Effects of alcohol on the development of the cardiovascular system in Pekin Ducks (Anasplatyrhynchos): An assessment of current empirical findings and the development of aresearch protocol utilizing Pekin Ducks." Capital University Honors Theses / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=caphonors1619709990242982.

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Heitkemper, Megan. "The Development of Computational Methods and Device Design Considerations Towards Improving Transcatheter Heart Valve Engineering." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595406932637358.

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Kouskouti, Christina [Verfasser], and Franz [Akademischer Betreuer] Kainer. "Short term fetal heart rate variation in intrauterine growth restriction : development of reference values for a new computational algorithm / Christina Kouskouti ; Betreuer: Franz Kainer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1170582702/34.

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Barnes, Amber K. "Zebrafish as a Model for Prenatal Alcohol Exposure: An Investigation Into Behavioral and Developmental Effects." University of Akron / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=akron1354306697.

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Pedersen, Cameron James. "Biophotonic Investigation of Cardiac Structure and Hemodynamics During Embryogenesis UsingOptical Coherence Tomography." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1575392583935489.

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Nogueira, Priscila Seravalli Calmon. "Sobrecarga e restrição de cloreto de sódio durante a gestação: repercussão sobre a estrutura cardíaca e renal no neonato." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-20052016-110245/.

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Introdução: Diversos estudos indicaram consequências de alterações na nutrição materna durante a gestação sobre a saúde da prole adulta, tais como: hipertensão, doenças cardiovasculares, resistência à insulina, diabete melito e doença renal. No entanto, a literatura é pobre em avaliações decorrentes de modificações nutricionais maternas sobre a prole logo após o nascimento. Métodos: Ratas Wistar durante o período gestacional foram alimentadas com dieta hipossódica (HO - 0,15% de NaCl), normossódica (NR - 1,3% de NaCl) ou hipersódica (HR - 8% de Na Cl). Após o nascimento, nas primeiras vinte e quatro horas foram coletados rins e coração dos neonatos machos e fêmeas (n=6- 8/grupo) para verificar as possíveis alterações na estrutura cardíaca e renal pelo método de estereologia. Também foi avaliada a expressão proteica e gênica dos componentes do sistema renina angiotensina (SRA) no coração e rins através do método ELISA indireto e RT-qPCR. Resultados: O peso ao nascimento foi menor em machos e fêmeas da prole de mães alimentadas com dieta hipossódica durante a gestação quando comparado NR e HR. Não houve diferença no volume renal, volume de seus compartimentos (córtex, medula e pelve) e número de glomérulos entre os grupos experimentais (HO, NR e HR). No entanto, o número de glomérulos foi maior em fêmeas comparado aos machos nos três grupos experimentais. O diâmetro transverso do núcleo dos cardiomiócitos no ventrículo esquerdo e no ventrículo direito de machos da prole HR foi maior do que na prole NR. A expressão proteica do receptor AT1 no rim de machos da prole foi menor no grupo HO do que no grupo NR e HR. A expressão proteica do receptor AT2 também foi menor em machos do grupo HO do que no grupo NR. Não houve diferença entre os grupos na expressão proteica dos receptores AT1 e AT2 no rim das fêmeas. Conclusão: O presente estudo detectou alterações na estrutura cardíaca de neonatos machos, mas não em neonatos fêmeas decorrentes de sobrecarga de sal durante a gravidez. As alterações observadas na expressão dos receptores AT1 e AT2 no rim de neonatos machos podem ser responsáveis por alterações na função renal
Introduction: Several studies have shown several consequences on adult offspring due to alterations in maternal nutrition during pregnancy, such as: hypertension, heart diseases, insulin resistance, diabetes mellitus and kidney diseases. Nevertheless, few studies evaluated maternal nutritional alterations in neonates. Methods: Female Wistar rats where fed from day one of pregnancy until delivery with low- (LS - 0.15% NaCl), normal- (NS - 1.3% NaCl) or high- (HS - 8%NaCl) salt diet. During the first twenty-four hours after birth, newborn\'s (n=6- 8/group) kidneys and heart were collected to evaluate possible changes of their structure by stereology. The protein and the gene expression of the renin angiotensin system components were evaluated by indirect ELISA and by RTqPCR, respectively. Results: Birth weight was lower in male and female offspring of dams fed LS during pregnancy. No differences between groups (LS, NS and HS) were observed in total renal volume and its compartments (cortex, medulla and pelvis) and number of glomeruli. The number of glomeruli was higher in female when compared to male newborns in the three experimental groups. The transverse diameter of the nuclei of the cardiomyocytes was higher in HS in both left and right ventricle vs. NS. The AT1 receptor protein expression was lower in kidneys of LS than in NS and HS male newborns. AT2 receptor protein expression was also lower in male LS than in NS. No differences in AT1 and AT2 receptors protein expression in female newborn\'s kidneys were found. Conclusion: The present study shows changes in cardiac structure male but not of female neonates induced salt overload during pregnancy. The alterations observed in AT1 and AT2 expression in kidneys of neonates may be responsible for alteration in renal function

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Books on the topic "Fetal heart development"

1

Jeffrey, Lipshitz, ed. Perinatal development of the heart and lung: Proceedings of the First International Christie Conference, Banff, Alberta, Canada. Ithaca, N.Y: Perinatology Press, 1987.

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J, Moss Arthur, and Allen Hugh D, eds. Moss and Adams' heart disease in infants, children, and adolescents: Including the fetus and young adult. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

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Karen, Bellenir, ed. Congenital disorders sourcebook: Basic information about disorders acquired during gestation, including spina bifida, hydrocephalus, cerebral palsy, heart defects, craniofacial abnormalities, fetal alcohol syndrome, and more, along with current treatment options and statistical data. Detroit, MI: Omnigraphics, 1997.

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J, Judd Sandra, ed. Congenital disorders sourcebook: Basic consumer health information about nonhereditary birth defects and disorders related to prematurity, gestational injuries, congenital infections, and birth complications, including heart defects, hydrocephalus, spina bifida, cleft lip and palate, cerebral palsy, and more; along with facts about the prevention of birth defects, fetal surgery and other treatment options, research initiatives, a glossary of related terms, and resources for additional information and support. 2nd ed. Detroit, MI: Omnigraphics, 2007.

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(Editor), Simcha Yagel, Norman H. Silverman (Editor), and Ulrich Gembruch (Editor), eds. Fetal Cardiography. Taylor & Francis, 2002.

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Monk, Catherine, and Amie Ashley Hane. Fetal and Infant Neurobehavioral Development. Edited by Amy Wenzel. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199778072.013.20.

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This chapter reviews the literature examining fetal and infant neurobehavioral development. Basic fetal neurological development and neurobehavioral functioning are reviewed. Major fetal neurobehavioral milestones and their assessment are addressed and include fetal behavioral states, heart rate, movement, and responsivity to stimuli. The processes of neurological growth from birth to age 2 are reviewed. Infant neurobehavioral development is addressed and includes state regulation and sleep, physical growth and motor development, and the basic processes underlying social-emotional development. For fetus and infant, research examining the associations between neurobehavioral development and maternal distress and poverty is reviewed. The implications for future directions in fetal-infant neurobehavioral research are discussed.

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Moss and Adams' Heart Disease in Infants, Children, and Adolescents : Including the Fetus and Young Adult (2 Volume Set). 6th ed. Lippincott Williams & Wilkins, 2001.

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J, Moss Arthur, Adams Forrest H, and Emmanouilides George C. 1926-, eds. Moss and Adams heart disease in infants, children, and adolescents: Including the fetus and young adult. 5th ed. Baltimore: Williams & Wilkins, 1995.

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Emmanouilides, George C., Arthur J. Moss, and Forrest H. Adams. Moss and Adams Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adult (2 Volume Set). 5th ed. Williams & Wilkins, 1995.

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1933-, Moller James H., and Neal William A. 1940-, eds. Fetal, neonatal, and infant cardiac disease. Norwalk, Conn: Appleton & Lange, 1990.

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Book chapters on the topic "Fetal heart development"

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Gonçalves, Hernâni, Diogo Ayres-de-Campos, and João Bernardes. "Linear and Nonlinear Analysis of Fetal Heart Rate Variability." In Fetal Development, 119–32. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22023-9_7.

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Van den Bergh, Bea R. H. "Maternal Anxiety, Mindfulness, and Heart Rate Variability During Pregnancy Influence Fetal and Infant Development." In Fetal Development, 267–92. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22023-9_14.

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Hoyer, D., and U. Schneider. "Fetal Development, Nonlinear Heart Rate Dynamics, and Self-Organization." In IFMBE Proceedings, 195–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03882-2_51.

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Price, Robert L., Jay D. Potts, Thomas E. Thielen, Thomas K. Borg, and Louis Terracio. "Growth Factor Regulation of Embryonic, Fetal, and Neonatal Cardiac Development." In Formation of the Heart and Its Regulation, 171–99. Boston, MA: Birkhäuser Boston, 2001. http://dx.doi.org/10.1007/978-1-4612-0207-3_10.

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Cohen, Meryl S. "Fetal Development and Prenatal Evaluation of Hypoplastic Left Heart Syndrome." In Developments in Cardiovascular Medicine, 9–28. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0253-1_2.

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Uv, Julie Johanne, Lena Myklebust, Hamid Khoshfekr Rudsari, Hannes Welle, and Hermenegild Arevalo. "3D Simulations of Fetal and Maternal Ventricular Excitation for Investigating the Abdominal ECG." In Computational Physiology, 13–24. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05164-7_2.

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AbstractCongenital heart disease (CHD) is a leading cause of infant death. To diagnose CHD, recordings from abdominal fetal electrocardiograms (fECG) can be used as a non-invasive tool. However, it is challenging to extract the fetal signal from fECG recordings partly due to the lack of data combining fECG recordings with a ground truth for the fetal signal, which can be obtained by using a scalp electrode during delivery. In this study, we present a computational model of a pregnant female torso, in which we simulate fetal and maternal ventricular excitation during sinus rhythm to derive fECGs, so as to enable isolated measurement of the fetal and maternal signal contributions. To extract the fetal contribution from a combined signal, we apply an adaptive filtering algorithm to wavelet transformed signals. Further development of the model may enable improvements in the recording and processing capabilities for fECGs, the reliable estimation of fetal heart rates, and possibly interpretation of fetal signal morphologies that could improve the overall diagnostic significance of abdominal fECGs.

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Pappano, Achilles J. "Development of Postjunctional Cardiac Autonomic Receptors and their Regulation of Cardiac Function during Fetal and Neonatal Life." In Physiology and Pathophysiology of the Heart, 381–411. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_18.

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Maeda, K. "Microcomputerized Automatic Fetal Heart Rate Monitoring as an External Method: Development of the Trendgram." In Gynecology and Obstetrics, 240–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70559-5_80.

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Thliveris, J. A., and J. Myers-Shrom. "Myocardial Changes in the Fetal Rat Heart Due to Stress During Prolonged Gestation." In Developments in Cardiovascular Medicine, 288–97. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2587-1_23.

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Schiaffino, Stefano, Simonetta Ausoni, Caterina Millino, Elisa Calabria, Claudia Sandri, and Raffaella Di Lisi. "A Cardiac-Specific Troponin I Promoter. Distinctive Patterns of Regulation in Cultured Fetal Cardiomyocytes, Adult Heart and Transgenic Mice." In Developments in Cardiovascular Medicine, 17–25. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-015-9321-2_3.

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Conference papers on the topic "Fetal heart development"

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Yalcin, Huseyin C., Huseyin E. Salman, and Reema Y. Kamal. "Assessment of Human Fetal Left Heart Hemodynamics during Prenatal Development." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0086.

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The hemodynamic forces and wall shear stresses (WSS) play an important role during the fetal heart development. Abnormal levels of flow-driven shear stress can deteriorate the proper functioning of the cells responsible for the growth and remodeling of the heart and lead to congenital heart defects (CHDs). Hypoplastic left heart syndrome (HLHS) is a critical CHD with severely underdeveloped left ventricle and responsible for 25-40% of all neonatal cardiac deaths. To characterize the main differences between the healthy and HLHS fetal hearts in terms of morphology, flow behavior, and WSS levels, will help to understand the mechanobiological development of the human fetal hearts. The comparison of healthy and HLHS fetal hearts is important to understand the embryonic development of HLHS. Computational fluid dynamics (CFD) modeling is performed to elucidate the flow behavior and WSS levels in the heart chambers. First, the model geometries are generated using the medical images. Then, the flow domain is discretized in spatial and time domains for solving the governing fluid flow equations. Inlet flow conditions are determined using the Doppler ultrasound velocity measurements. The analyses cover the range of gestational week 16 and week 34. HLHS hearts have higher peak flow rates at the valves compared to the control hearts. The turbulent activity in the left side of the heart is higher than the right side. For the control hearts, there is a balance between the left and right sides of the heart, which is preserved during the development. The ratio of the cross-sectional area between the left and right sides of the heart is about 57.5% to 42.5% for the control hearts. HLHS significantly reduces the cross-sectional area of the left side of the heart. For HLHS hearts, the ratio between the left and right sides becomes about 30% to 70%. The average WSS levels significantly increase at the left side of the HLHS hearts. This study indicates the critical importance of the altered inflow hemodynamics during the human fetal heart development. CFD analysis can be used to predict the initiation and growth of CHDs. The presence of CHDs significantly changes the biomechanical environment in the fetal hearts.

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Rotariu, Cristian, Alexandru Pasarica, Hariton Costin, and Dragos Nemescu. "Spectral analysis of fetal heart rate variability associated with fetal acidosis and base deficit values." In 2014 International Conference on Development and Application Systems (DAS). IEEE, 2014. http://dx.doi.org/10.1109/daas.2014.6842457.

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Cysarz, Dirk, Friedrich Edelhauser, and Peter Van Leeuwen. "Binary Symbolic Dynamics of Fetal Heart Rate Reflects Individual Gestational Development." In 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847506.

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Hoyer, Dirk, Alexander Schmidt, Kathleen Gustafson, and Uwe Schneider. "From Darwin to Monitoring the Fetal Development - a Multi-Score using Categories of Heart Rate Patterns." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158189.

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Dodson, Reuben B., Kendall S. Hunter, and Virginia L. Ferguson. "Elastic Properties of the Human Umbilical Cord in Preeclampsia." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53673.

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Maternal diseases of pregnancy have been found to detrimentally affect the fetal circulatory system, with consequences lasting well into adulthood. In 1995, Barker introduced the idea that major disorders of adult life (including coronary heart disease, hypertension, stroke and diabetes) arise not only through an interaction between factors in our lifestyle, such as a high-fat diet, obesity and smoking, and a genetically determined susceptibility but also through development in utero [1]. Epidemiological evidence continues to support the notion that adult cardiovascular disease (CVD) has fetal origins [2–5].

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Fu, Luoyu, Peiqi Yi, Zikun Gao, and Yan Gan. "Design and Research of Flexible Wearable Medical Testing Equipment for Pregnant Women." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001478.

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Pregnant women, as a special group, bear the mission of nurturing and continuing human life. Pregnant women need to experience psychological and physiological changes in the tenth month of pregnancy. In the special "post-epidemic era", it is hard and unsafe for pregnant women to go to the hospital regularly for birth check-up. In order to make pregnant women have a better prenatal experience, our team wants to design a wearable device, which can monitor the fetal heart rate and the frequency of fetal movement, so that pregnant women can also realize routine detection of the fetal condition at home, and protect the growth health and safety of the fetus. In this design, questionnaire interview, literature search and collaborative story telling are used to deeply understand the pain points of pregnant women's antenatal examination, the development status of wearable devices for pregnant women at home and abroad, pregnant women's preferences and so on. Then, determine the product use process, product functional structure and product packaging. This design adopts cutting-edge technologies such as flexible sensors, and combines ergonomics and kansei engineering. The product obtains the data and information of pregnant women and fetuses, and then through sorting and analysis, the results are intuitively transmitted to pregnant women, pregnant women's relatives or doctors in the matching APP, so that users can clearly obtain the health data of pregnant women in real time. Realize early warning of physical abnormalities of infants and mothers, early warning and early treatment, so as to better protect the safety and health of pregnant women and fetuses during pregnancy. After the usability test, the interviewed pregnant women thought that the design had a certain effect.

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Hoyer, D., S. Nowack, and U. Schneider. "Multi-scale characteristics of resampled fetal heart rate pattern provide novel fetal developmental indices." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090336.

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Menon, Prahlad G., William Kowalski, and Kerem Pekkan. "Computational Fluid Dynamics Analysis of Early Embryonic Aortic Arch-Ligation." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14470.

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Congenital heart disease occurs in 8 out of every 1000 live births in the US and more than half of this population is associated with great artery lesions. Selective remodeling of the paired, bilaterally symmetric embryonic aortic arches (AA) is a crucial stage in vascular morphogenesis and has known association with biomechanical forces [1]. Fetal cardiac interventions are currently explored clinically as an alternative repair technique for congenital anomalies, in-utero [2]. Several computational fluid dynamics (CFD) studies have been performed focusing on subject specific embryonic cardiovascular anatomies [3–5]. These developments could benefit fetal interventions that are planned in-silico before execution. To demonstrate this possibility, we computed the hemodynamic variation and wall shear stress (WSS) patterns resulting from systematic in-silico AA ligation intervention performed on normal chick AA models viz. Hamburger Hamilton (HH) stage 18 and 24 (3 and 4 days, respectively). A unique methodology employing CFD-computed WSS for modeling short-term biological growth response on AA morphogenesis is also presented.

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Reports on the topic "Fetal heart development"

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Halevy, Orna, Zipora Yablonka-Reuveni, and Israel Rozenboim. Enhancement of meat production by monochromatic light stimuli during embryogenesis: effect on muscle development and post-hatch growth. United States Department of Agriculture, June 2004. http://dx.doi.org/10.32747/2004.7586471.bard.

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The original objectives were: A. To determine the critical embryonic age for monochromatic green light stimulation. B. To follow the ontogeny of embryos exposed to monochromatic green light vs. darkness. C. To investigate the effects of monochromatic green light illumination on myoblast and fiber development in the embryo. D. To investigate the stimulatory effect of light combinations during embryo and post-hatch periods on growth and meat production. E. To evaluate the direct effect of monochromatic green light on cultured embryonic and adult myoblasts. The overall purpose of this study was to investigate the effect of monochromatic light stimuli during incubation period of broilers on muscle development and satellite cell myogenesis. Based on previous studies (Halevy et al., 1998; Rozenboim et al., 1999) that demonstrated the positive effects of green-light illumination on body and muscle growth, we hypothesized that monochromatic light illumination accelerates embryo and muscle development and subsequently enhances muscle growth and meat production. Thus, further decreases management costs. Under the cooperation of the laboratories at the Hebrew University of Jerusalem and University of Washington we have conducted the following: 1. We have established the critical stage for exposure to green monochromatic light which has the maximal effect on body and muscle growth (Objective A). We report that embryonic day 5 is optimal for starting illumination. The optimal regime of lighting that will eliminate possible heat effects was evaluated by monitoring egg core temperature at various illumination periods. We found that intermitted lighting (15 min. on; 15 min. off) is optimal to avoid heat effects. 2. We have evaluated in detail gross changes in embryo development profile associated to green light stimuli vs. darkness. In addition, we have investigated the stimulatory effect of light combinations during embryo and post-hatch periods on body and muscle growth (Objective B,D). 3. We have studied the expression profile of muscle regulatory proteins during chicken muscle cell differentiation in cultures using newly developed antibodies. This study paved the way for analyzing the expression of these proteins in our photo stimulation experiments (Objective C). 4. We have studied the pattern ofPax7 expression during myogenesis in the posthatch chicken. Experimental chick pectoralis muscles as well adult myoblast cultures were used in this study and the results led us to propose a novel model for satellite cell differentiation and renewal. 5. The effects of monochromatic green light illumination during embryogenesis have been studied. These studies focused on fetal myoblast and satellite cell proliferation and differentiation at pre- and posthatch periods and on the effects on the expression of muscle regulatory proteins which are involved in these processes. In addition, we have analyzed the effect of photo stimulation in the embryo on myofiber development at early posthatch (Objective C). 6. In follow the reviewers' comments we have not conducted Objective E. The information gathered from these studies is of utmost importance both, for understanding the molecular basis of muscle development in the posthatch chicks and for applied approach for future broiler management. Therefore, the information could be beneficial to agriculture in the short term on the one hand and to future studies on chick muscle development in the embryo and posthatch on the other hand.

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