Augmentation of coronary conductance in adult sheep made anaemic during fetal life

Davis, Lowell E.; Roullet, Jean-Baptiste; Thornburg, Kent L.; Shokry, Meray M.; Hohimer, A. Roger; Giraud, G

doi:10.1111/j..2002.00053.x

Cited by 25 publications

(36 citation statements)

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“…Experimental evidence that intrauterine influences can have persisting effects on the coronary circulation has come from studies of sheep that were made anemic during fetal life. 16 Adult sheep that in utero had been made anemic by isovolemic hemorrhage for a 10-day period in late gestation showed greater maximal conductance in the coronary circulation. 16 Fetal anemia led to increased coronary reserve and a greater cardiac functional response to acute hypoxic stress in the adult sheep.…”

Section: Discussionmentioning

confidence: 99%

“…16 Adult sheep that in utero had been made anemic by isovolemic hemorrhage for a 10-day period in late gestation showed greater maximal conductance in the coronary circulation. 16 Fetal anemia led to increased coronary reserve and a greater cardiac functional response to acute hypoxic stress in the adult sheep. 17 Intrauterine influences on the development of the coronary circulation of human infants could have important implications.…”

Section: Discussionmentioning

confidence: 99%

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Birth Weight and Cardiac Structure in Children

et al. 2006

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OBJECTIVE. Epidemiologic studies have shown associations between impaired fetal growth and risk for coronary heart disease in adults. The underlying mechanisms are unknown. We investigated whether restricted intrauterine growth affects cardiac structure.METHODS. We performed echocardiography on 216 9-year-old children who were measured previously at birth. The diameter of the coronary left and right main branches was derived from the widest dimension; total coronary artery diameter was calculated by adding the diameters of the left and right coronary arteries. Aortic root diameter, left atrial diameter, left ventricular diameter, left ventricular outflow tract diameter, and left ventricular mass were measured.RESULTS. On average, children who had weighed less at birth had a smaller total coronary artery diameter, aortic root diameter, and left ventricular outflow tract diameter after adjustment for gender, gestational age, current height and weight, and maternal height and prepregnant weight. For each SD increase in birth weight, total coronary diameter rose by 0.10 mm, log aortic root diameter rose by 1.5%, and log left ventricular outflow tract diameter rose by 1.6%.CONCLUSION. Impaired fetal growth may have long-term effects on cardiac structure. This may help to explain why adults whose birth weight was low are at greater risk for coronary heart disease. [1][2][3][4][5] The mechanisms that underlie this relation are unclear. One possibility may be that poor fetal growth has effects on cardiac structure that persist into childhood and beyond, increasing the risk for coronary artery disease.We used echocardiography to examine a group of 216 children who were aged 9 years and had been measured at birth. Our aim was to investigate the relation between birth weight and cardiac chamber, aortic root, and coronary artery diameters. METHODSThe mothers of the children in this study all had taken part in an earlier study of nutrition during pregnancy between April 1992 and June 1993. White women who were aged 16 years or more and had singleton pregnancies of Ͻ17 weeks' gestation were recruited during their first visit to the midwives' antenatal booking clinic at the Princess Anne Maternity Hospital in Southampton, UK; women who had diabetes and those who had undergone hormonal treatment to conceive were excluded. There were routine obstetric data about the pregnancy and delivery, and anthropometric data on the child were collected at birth. Gestation was estimated from menstrual history and scan data. 6 In total, 559 children were followed up to the age of 9 months, and these children form the sampling frame for this study.When the children approached 9 years of age, we asked the Community Pediatric Service in Southampton to write to their parents with an invitation to take part in an additional follow-up study to investigate the effect of early growth on the structure and function of the heart and blood vessels, on cognitive function, and on bone mass. We chose to study the children at 9 years of age because ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Birth Weight and Cardiac Structure in Children

et al. 2006

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“…There is recent evidence suggesting that growth of the myocardial vasculature in the fetus may be affected by perturbations in utero (13). Under normal conditions, the rate of coronary vascularization during development is regulated by the magnitude of cardiac growth (14).…”

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confidence: 99%

“…Under normal conditions, the rate of coronary vascularization during development is regulated by the magnitude of cardiac growth (14). However, hypoxia is a strong stimulus of capillary growth (15), and recent studies suggest that hypoxia in utero may augment the growth of the myocardial vasculature (13). Whether maternal protein restriction affects the vascularization of the heart is currently unknown.…”

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confidence: 99%

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Effect of Maternal Protein Restriction in Rats on Cardiac Fibrosis and Capillarization in Adulthood

2006

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This study examines the effect of maternal protein restriction in rats on levels of cardiac fibrosis, myocardial capillarization, and media:lumen ratio of intramyocardial arteries in adult offspring. Female Wistar Kyoto rats were fed either a normal protein diet (NPD; 20% casein) or a low-protein diet (LPD; 8.7% casein) during pregnancy and lactation. Female offspring (seven per group) were weaned at 4 wk of age and grown to adulthood. At 24 wk of age, the offspring were perfusion fixed. Cardiac fibrosis and media:lumen ratio of intramyocardial arterioles was assessed using image analysis and cardiac capillarization was stereologically investigated. Body weights at 2 and 24 wk of age were significantly reduced (31% and 8%, respectively) in the LPD offspring; however, heart size was not different at 24 wk. Importantly by adulthood, there was a significant 15% increase in left ventricular interstitial fibrosis in LPD offspring. There were no differences in levels of perivascular fibrosis, myocardial capillarization, or in the media:lumen ratio of intramyocardial arteries between groups. Because cardiac fibrosis is associated with impaired cardiac contractility and arrhythmia, our results suggest that induction of interstitial fibrosis may contribute to the increased cardiac disease in adult subjects who were exposed to an adverse intrauterine environment. M any epidemiologic studies have shown that subjects exposed to perturbations in early development have an increased incidence of cardiovascular disease later in life (1-3). It is likely that an adverse intrauterine environment may permanently reduce the numbers of cells/functional units in vital organs, which in turn will affect postnatal organ function. Recent experimental studies of reduced nephron endowment in kidneys, as a result of maternal protein restriction, and subsequent detrimental effects on renal function later in life support this concept (4); whether this is the case in the heart has not yet been elucidated. Interestingly in a recent study in our laboratory, we found that maternal protein restriction throughout pregnancy in rats leads to a reduced heart size and a concomitant decrease in the number of cardiomyocytes (5). Because cardiomyocytes in general cease proliferating soon after birth, with postnatal growth of the heart predominantly due to cardiomyocyte hypertrophy (6), these findings could have important adverse implications on the structure and function of the heart later in life. We postulate that a decrease in the total number of cardiomyocytes in neonatal hearts will limit the capacity for physiologic cardiac growth in adulthood. We propose that when cardiomyocytes reach their limits of hypertrophy, further enlargement of the heart will then occur through increased deposition of extracellular matrix leading to cardiac fibrosis.Indeed, accumulation of extracellular matrix structural proteins in the heart adversely affects myocardial viscoelasticity (7,8) with accumulation of fibrillar collagen leading to cardiac dysfunction (9...

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2013

Nutrition and Development

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Augmentation of coronary conductance in adult sheep made anaemic during fetal life

Cited by 25 publications

References 18 publications

Birth Weight and Cardiac Structure in Children

Birth Weight and Cardiac Structure in Children

Effect of Maternal Protein Restriction in Rats on Cardiac Fibrosis and Capillarization in Adulthood

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