Umbilical artery flow velocity waveforms and placental resistance: The effects of embolization of the umbilical circulation

Trudinger, Brian J.; Stevens, Denise; Connelly, Anita; Hales, J. R. S.; Alexander, G.; Bradley, Laurence A.; Fawcett, A. A.; Thompson, R.S.

doi:10.1016/s0002-9378(87)80241-7

Cited by 246 publications

(95 citation statements)

References 10 publications

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“…UPE has been shown to increase the vascular resistance of the placenta (14) by obstructing placental vessels and it may, therefore, increase the total peripheral resistance of the fetoplacental circulation. In contrast, arterial pressures in our postnatal IUGR lambs were lower than in controls suggesting that their total peripheral resistance may have been reduced by UPE.…”

Section: Discussionmentioning

confidence: 99%

“…We have used the UPE technique as it is a controllable and reproducible means of restricting placental function that results in IUGR. Furthermore, many of its effects in the sheep have been documented (12)(13)(14) and resemble features of growth restricted human fetuses (15). We have measured plasma cortisol and renin as these hormones have been implicated in the regulation of blood pressure (16,17).…”

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confidence: 99%

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Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

et al. 2000

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Low birth weight has been associated with elevated arterial pressure in later life but mechanisms are unknown. Our aim was to determine the effects of low birth weight resulting from intrauterine growth restriction (IUGR) on fetal and postnatal arterial pressures and the potential roles of circulating cortisol and renin. We induced IUGR by umbilico-placental embolization (UPE) in fetal sheep from 120 d of gestation until birth (approximately 147 d); postnatal lambs (8 IUGR, 8 controls) were studied for 8 wk. Fetal and postnatal arterial pressures were measured and blood samples taken for measurement of gas tensions, cortisol concentrations and renin activity. In IUGR fetuses, mean arterial pressure (MAP) initially increased with UPE, but near term was not different to values in controls. IUGR lambs weighed 33% less than controls at birth and remained lighter than controls during the 8 postnatal weeks; their growth pattern was different to that of controls. IUGR lambs had lower MAP than controls, and this relative hypotension (Ϫ4 mm Hg) persisted throughout the 8 postnatal weeks. Covariate analysis showed that the relative hypotension of IUGR lambs could have resulted from their smaller size. Plasma cortisol concentrations were not different between IUGR and control animals before or after birth. Plasma renin activity was not different in postnatal IUGR lambs compared with controls. Thus, postnatal cortisol and renin levels were not consistent with the development of hypotension or hypertension. We conclude that late gestational IUGR in sheep leads to relative hypotension in the early postnatal period, probably a result of reduced body size. There is increasing evidence that low birth weight resulting from intrauterine growth restriction (IUGR) is associated with an increased risk of later illness. Associations have been demonstrated between low birth weight and an increased risk of adult-onset diseases such as hypertension, coronary heart disease and type II diabetes (1, 2). In adults, an inverse relationship has been found between arterial pressure and birth weight (3, 4) and this relationship has been found to be independent of current body size and lifestyle factors (1). Studies in children have also revealed inverse relationships between birth weight and arterial pressure (5). The relationship in adolescents is less clear with some studies finding inverse relationships between birth weight and arterial pressure (6) and others finding positive relationships (7). Based on epidemiologic findings, it has been proposed that hypertension is initiated in utero and is amplified with age (8).Several studies of fetal growth restriction in animals have also shown relationships between a sub-optimal intrauterine environment and arterial pressure. Mid-gestational uterine artery ligation in guinea pigs has been shown to produce growth restricted offspring with an elevated mean arterial pressure (9). In the rat, a low protein diet during pregnancy also leads to growth restricted offspring with an elevated systolic pressure...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

et al. 2000

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“…the dependence of the angle between the ultrasound beam and the direction of flow in the vessel. These indices, recorded from the umbilical artery, have been found to correlate with placental vascular resistance ( 18,19) and placental microvascular pathology (20) but have not been validated as markers of fetal cerebral vascular resistance or flow. A positive correlation has, however, been demonstrated between internal carotid PI and fetal O2 tension (21).…”

Section: Discussionmentioning

confidence: 99%

Effects of Increased Resistance to Umbilical Blood Flow on Fetal Hemodynamic Changes Induced by Maternal Oxygen Administration: A Doppler Velocimetric Study on the Sheep

et al. 1993

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ABSTRACT. A fetal lamb model was used to investigate whether the effects of maternal O2 administration on fetal blood gases and hemodynamics were modified when the fetoplacental circulation was compromised by stepwise compression of both umbilical veins. At basal state, O2 administration increased O2 saturation (Sao2) and the pulsatility index (PI) of the carotid artery Doppler wave form ( p < 0.01). The first compression decreased left ventricular output (-21 + 16%, mean + 1 SD, p < 0.01) and umbilical mean velocity (-22 + 28%, p < 0.01) but did not modify carotid pH, Sao2, or the PI in any of the arteries studied. At this level of compression, O2 administration increased carotid Sao2 ( p < 0.01) but did not affect carotid PI. After a second compression, left ventricular output and umbilical mean velocity were even more reduced 1-39 f 21% ( p < 0.01) and -53 f 23% ( p < 0.01), respectively]. With this compression, carotid pH, Sao2, and PI decreased, whereas umbilical and descending aorta PI increased. O2 administration at this level of compression increased carotid Sao2 ( p < 0.01) but did not modify carotid PI.

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“…We induced FGR by UPE as it replicates key features of human FGR (13,14) and the metabolic, cardiovascular, and endocrine effects of UPE have been defined (15)(16)(17). Our hypothesis was that changes in lung development induced by placental insufficiency and FGR during late gestation, coinciding with the saccular and alveolar phases of lung development, persist into adulthood.…”

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Fetal Growth Restriction Has Long-Term Effects on Postnatal Lung Structure in Sheep

et al. 2004

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We have previously shown that fetal growth restriction (FGR) during late gestation in sheep affects lung development in the near-term fetus and at 8 wk after birth. In the present study, our aim was to determine the effects of FGR on the structure of the lungs at 2 y after birth; our hypothesis was that changes observed at 8 wk after birth would persist until maturity. FGR was induced in sheep by umbilicoplacental embolization, which was maintained from 120 d until delivery at term (approximately 147 d); birth weights of FGR lambs were 41% lower than in controls. At 2 y after birth, body and lung weights were not different, but there were 28% fewer alveoli and alveoli were significantly larger than in controls; hence there was a 10% reduction in the internal surface area relative to lung volume in FGR sheep compared with controls. The lungs of FGR sheep, compared with controls, had thicker interalveolar septa as a result of increased extracellular matrix deposition; the alveolar blood-air barrier was also thicker, largely because of an 82% increase in basement membrane thickness. These changes are qualitatively similar to those observed at 8 wk. Our data show that structural alterations in the lungs induced by FGR that were apparent at 8 wk were still evident at 2 y after birth, indicating that FGR may result in permanent changes in the structure of the lungs of the offspring and may affect respiratory health and lung aging later in life. Low birth weight as a result of FGR has been associated with an increased risk of morbidity and mortality during infancy (1, 2). It is likely that altered lung development may be a contributing factor as it has been shown that the risk of respiratory illness and the requirement for ventilatory support is increased in FGR infants (3, 4). Respiratory impairments may persist into later life because low birth weight children who were growth-restricted in utero (5, 6), as well as adults having low birth weights (7,8), have evidence of impaired lung function. At present, however, the structural basis for a relationship between FGR and later pulmonary dysfunction is poorly understood.The sheep is a suitable animal model in which to study the effects of FGR on lung development; it is a long-gestation species in which alveolar formation begins before birth (9), as in the human (10), and which reaches sexual maturity 6 mo after birth. Recently we found, in developing sheep, that fundamental aspects of respiratory function were impaired after FGR; FGR lambs were hypoxemic and hypercapnic soon after birth and had reduced pulmonary diffusing capacity and lung compliance up to 8 wk (11). In addition to these functional alterations, we found that FGR induced structural changes in lung parenchyma that were evident in the near-term fetus and became more pronounced at 8 wk after birth (12). In particular, the blood-air barrier and structure of interalveolar septa were affected after FGR. It is possible that structural

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Umbilical artery flow velocity waveforms and placental resistance: The effects of embolization of the umbilical circulation

Cited by 246 publications

References 10 publications

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

Effects of Increased Resistance to Umbilical Blood Flow on Fetal Hemodynamic Changes Induced by Maternal Oxygen Administration: A Doppler Velocimetric Study on the Sheep

Fetal Growth Restriction Has Long-Term Effects on Postnatal Lung Structure in Sheep

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