Chronic fetal placental embolization and hypoxemia cause hypertension and myocardial hypertrophy in fetal sheep

Murotsuki, Jun; Challis, John; Han, V. K. M.; Fraher, L. J.; Gagnon, Robert

doi:10.1152/ajpregu.1997.272.1.r201

Cited by 79 publications

(110 citation statements)

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“…The mechanism by which this occurs is unknown. Elevated blood pressure can cause cardiac hypertrophy possibly by increasing afterload to the heart (Murotsuki et al 1997).…”

Section: Fetal Growthmentioning

confidence: 99%

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Jensen¹,

Gallaher²,

Breier³

et al. 2002

Journal of Endocrinology

114

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Exposure of the fetus to excess maternal glucocorticoids has been postulated to alter fetal growth and development, and thus provide a possible mechanism for the link between impaired fetal growth and altered postnatal physiology. However, the effects of exposure to excess maternal glucocorticoids on fetal physiology and metabolism in utero have not been described. We therefore studied the effects of chronic maternal cortisol infusion on fetal growth, blood pressure, metabolism and endocrine status in chronically catheterised fetal sheep. We infused hydrocortisone (80 mg/day, n=6) or saline (n=8) for 10 days into the pregnant ewes beginning at 119 days of gestation. Maternal cortisol infusion reduced fetal growth rate by 30% (girth increment 2·9 0·3 vs 1·8 0·4 mm/ day, P=0·03). Maternal cortisol infusion increased fetal heart weight by 15% relative to body weight and increased ventricular wall thickness by 30% in the left and 50% in the right ventricle. The weight of the spleen was reduced by 30% and placental weight reduced by 25%. Fetal blood pressure increased by approximately 10 mmHg (20%) during maternal cortisol infusion.Maternal cortisol infusion did not alter amino-nitrogen concentrations. However, maternal lactate concentrations increased by 80% and fetal lactate concentrations increased by 74% with maternal cortisol infusion, and both maternal and fetal urea concentrations increased by 40%. Circulating maternal IGF-binding protein (IGFBP)-3 levels had increased by 20% by the end of the maternal cortisol infusion. Fetal IGF-I concentrations decreased during cortisol infusion and fetal IGFBP-1 concentrations were negatively correlated with fetal weight (r= 0·76, P=0·02).We conclude that even a modest elevation of maternal cortisol levels affects fetal growth, cardiovascular function, metabolism and endocrine status which may have longterm consequences.

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“…The mechanism by which this occurs is unknown. Elevated blood pressure can cause cardiac hypertrophy possibly by increasing afterload to the heart (Murotsuki et al 1997).…”

Section: Fetal Growthmentioning

confidence: 99%

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Jensen¹,

Gallaher²,

Breier³

et al. 2002

Journal of Endocrinology

114

View full text Add to dashboard Cite

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“…Intrauterine growth retardation is associated with increased neonatal mortality, perinatal complications and long-term neurologic sequelae in preterm infants (1), as well as compromised cardiovascular adaptive capacity already in utero (2)(3)(4). However, few data have been reported regarding early circulatory adaptation after intrauterine growth retardation.…”

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confidence: 99%

Cardiac Hypertrophy and Altered Hemodynamic Adaptation in Growth-Restricted Preterm Infants

et al. 2003

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The objective was to elucidate hemodynamic adaptation in very low birth weight (Ͻ1500 g) infants after intrauterine growth retardation. 31 growth-retarded (SGA, birth weight Ͻ-2 SD) and 32 appropriate for gestational age (AGA, birth weight within Ϯ 1 SD range) infants were enrolled. In SGA infants, the diastolic diameters of the interventricular septum and the left ventricle were increased, and serum brain natriuretic peptide (BNP) was elevated. Left ventricular output (LVO) of the AGA infants increased from 150 Ϯ 28 to 283 Ϯ 82 mL/kg/min during the study (p Ͻ 0.01). The SGA infants had a higher initial LVO than the AGA infants (243 Ϯ 47 versus 150 Ϯ 28 mL/kg/min, p Ͻ 0.05), but did not show further LVO increase during the study period. Red cell (RCV) and blood (BV) volume were assessed by Hb subtype analysis, when packed donor red cells were transfused. RCV and BV did not differ between the groups initially, but RCV increased by 18% and BV by 29% in the AGA group during the first 3 d. On day 3, AGA infants had larger BV than the SGA infants (88 Ϯ 5 versus 73 Ϯ 12 mL/kg, p Ͻ 0.05). In conclusion, cardiac hypertrophy, elevated initial LVO and BNP of the SGA infants suggest increased cardiac workload after intrauterine growth retardation. Based on the BV and RCV data, blood volume regulation may also be impaired. The data suggest that SGA preterm infants may be exposed to an increased risk of circulatory failure during early adaptation. Intrauterine growth retardation is associated with increased neonatal mortality, perinatal complications and long-term neurologic sequelae in preterm infants (1), as well as compromised cardiovascular adaptive capacity already in utero (2-4). However, few data have been reported regarding early circulatory adaptation after intrauterine growth retardation. In addition to myocardial performance, adequate intravascular volume is essential for successful postnatal cardiovascular adaptation. Largely due to the lack of applicable methodology, present knowledge on intravascular volume of preterm infants in general is scarce, and the effect of growth retardation on circulating volume has not been studied.The aim of the present study was to test the hypothesis that fetal growth retardation alters the pattern of early hemodynamic adaptation of very low birth weight infants. During the first two weeks of life, left ventricular function and dimensions were assessed by echocardiography in SGA infants and AGA control infants. A circulating indicator of ventricular dysfunction, BNP, was also measured. RCV and BV were determined by a method based on dilution of autologous HbF by donor HbA when red cells were transfused based on clinical judgment. Hemodynamic evaluation was also performed by using indirect indices applied in routine clinical work. METHODS Patients.All infants in the study were born in the maternal unit of the Helsinki University Hospital and treated in the

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“…Animal studies have demonstrated that placental insufficiency-induced IUGR leads to decreases in oxygenation and substrate availability for the fetus [41][42][43]. Therefore, the uterine ligation or uterine ablation serves as an excellent model for examining idiopathic IUGR and the short-and long-term effects on liver function.…”

Section: Uterine Ligation or Ablation Model Of Undernutrition And Lonmentioning

confidence: 99%

Maternal Undernutrition and Long-Term Effects on Hepatic Function

Hardy

2017

Diet, Nutrition, and Fetal Programming

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Chronic fetal placental embolization and hypoxemia cause hypertension and myocardial hypertrophy in fetal sheep

Cited by 79 publications

References 0 publications

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Cardiac Hypertrophy and Altered Hemodynamic Adaptation in Growth-Restricted Preterm Infants

Maternal Undernutrition and Long-Term Effects on Hepatic Function

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