Amniotic fluid catecholamines and metabolites in intrauterine growth retardation

Divers, Walter A.; Wilkes, Mahlon M.; Babaknia, A.; Hill, Lyndon M.; Quilligan, Edward J.; Yen, S. S. C.

doi:10.1016/s0002-9378(15)33298-1

Cited by 26 publications

(11 citation statements)

References 17 publications

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“…In addition, the delayed maturation of the fetal lungs during a diabetic pregnancy may be due to decreased sympathoadrenal activity [12]. Previous and present results also show that there is a positive correlation between am niotic fluid phospholipids and catechol amines [13,14], The accelerated pulmonary maturation observed in growth-retarded fe tuses [10] and fetuses of mothers during the process of methadone withdrawal is probably due to the hyperactivity of fetal sympathetic nervous system [5].…”

Section: Discussionsupporting

confidence: 55%

“…The clinical significance of this finding is unclear. According to Diverset al [10] the fetal adren ergic system is hyperactive in fetal growth retardation, frequently associated with ma ternal hypertension. In our series the mean amniotic fluid NE concentration of patients with a growth-retarded fetus was not higher than in control subjects.…”

Section: Discussionmentioning

confidence: 99%

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Amniotic Fluid Norepinephrine Concentration as an Indicator of Fetal Sympathetic Nervous Activity

Puolakka¹,

Kauppila²,

Vuori³

1984

Gynecol Obstet Invest

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The concentrations of norepinephrine in amniotic fluid and maternal plasma were measured in 71 third trimester pregnancies, 31 of which were uncomplicated and 40 complicated. The amniotic fluid norepinephrine concentration (mean ± SD) in cases of hypertension treated with clonidine (0.4 ± 0.1 ng/ml, n = 12) and in insulin-dependent diabetes (0.5 ± 0.2 ng/ml, n = 7) was lower, and in renal insufficiency (1.7 ± 0.8 ng/ml, n = 8) higher than in control subjects (0.7 ± 0.4 ng/ml, n = 31). In fetal-growth retardation (0.6 ± 0.2 ng/ml, n = 8) and in latent diabetes (0.7 ± 0.2 ng/ml, n = 5) the values were similar to those in the control subjects. There was a significant positive correlation between mature lecithin-sphingomyelin (L/S) ratio and norepinephrine concentration. Clonidine-treated hypertension was associated with decreased (0.2 ± 0.1 ng/ml) and renal insufficiency with increased (0.9 ± 0.7 ng/ml) maternal plasma norepinephrine concentrations (control group, 0.3 ± 0.1 ng/ml). The present results indicate that measurement of catecholamines in amniotic fluid can be useful in the evaluation of fetal sympathoadrenal function.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Amniotic Fluid Norepinephrine Concentration as an Indicator of Fetal Sympathetic Nervous Activity

Puolakka¹,

Kauppila²,

Vuori³

1984

Gynecol Obstet Invest

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“…The poor amount of oxygen and substrates provided Severi/Rizzo/Bocchi/D'Antona/Verzuri/ Arduini causes a simultaneous circulation adaptation response which initially manifests through an increase of the blood flow in the ductus venosus in order to increase the oxygenated blood to the heart [17]. When the fetus undergoes metabolic stress, it reacts with an anti-insulin response probably regulated by the catecholamines, high levels of which have been documented in the amniotic fluid [18]. The catecholamines determine a reduction of the fat and glycogen deposits, as well as of the muscular mass, and they probably regulate the redistribution of the heart output with an increase of the blood flow to the brain, heart and glandula suprarenalis and a simultaneous peripheral vasoconstriction (viscera and muscles).…”

Section: Uteroplacental Insufficiencymentioning

confidence: 99%

Intrauterine Growth Retardation and Fetal Cardiac Function

Severi¹,

Rizzo

Bocchi³

et al. 2000

Fetal Diagn Ther

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Intrauterine growth retardation is a pathology which is found in 3–10% of all pregnancies and it is associated with around 20–25% of all fetal intrauterine deaths and with long-term neurologic sequelae. It presents an increased risk of distress during labor and delivery and a greater risk of perinatal mortality. The causes of IUGR and the cardiac and venous Doppler in normal fetuses are analyzed, and the hemodynamic cardiac modifications in IUGR fetus are discussed. The fetal cardiac function in intrauterine growth retardation shows a redistribution of the fetal cardiac output, which tends to favor the left ventricle as the mechanism to compensate for the uteroplacental insufficiency. The Doppler velocity indices are modified as the fetal condition progressively deteriorates and they represent an important tool for the management of the complicated pregnancy.

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“…Impaired insulin secretion is associated with a diabetic phenotype indicating that in utero complications can permanently compromise ␤-cell development and function (27,28). A fetal sheep model with placental insufficiency-induced intruterine growth restriction shares many similarities with human IUGR fetuses, such as asymmetric growth, hypoxemia, hypoglycemia, hypoinsulinemia, and hypercatecholaminemia [epinephrine and norepinephrine (NE)] (4, 16,18,22,23,32,41,47). Furthermore, glucose-stimulated insulin secretion (GSIS) and ␤-cell mass are lower in IUGR sheep fetuses, which also replicate features in human IUGR fetuses (34 -36, 41, 53).…”

mentioning

confidence: 99%

Enhanced insulin secretion responsiveness and islet adrenergic desensitization after chronic norepinephrine suppression is discontinued in fetal sheep

Chen

Green

Macko

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Chen X, Green AS, Macko AR, Yates DT, Kelly AC, Limesand SW. Enhanced insulin secretion responsiveness and islet adrenergic desensitization after chronic norepinephrine suppression is discontinued in fetal sheep. Am J Physiol Endocrinol Metab 306: E58 -E64, 2014. First published November 19, 2013 doi:10.1152/ajpendo.00517.2013.-Intrauterine growth-restricted (IUGR) fetuses experience prolonged hypoxemia, hypoglycemia, and elevated norepinephrine (NE) concentrations, resulting in hypoinsulinemia and ␤-cell dysfunction. Previously, we showed that acute adrenergic blockade revealed enhanced insulin secretion responsiveness in the IUGR fetus. To determine whether chronic exposure to NE alone enhances ␤-cell responsiveness afterward, we continuously infused NE into fetal sheep for 7 days and, after terminating the infusion, evaluated glucose-stimulated insulin secretion (GSIS) and glucose-potentiated arginine-induced insulin secretion (GPAIS). During treatment, NE-infused fetuses had greater (P Ͻ 0.05) plasma NE concentrations and exhibited hyperglycemia (P Ͻ 0.01) and hypoinsulinemia (P Ͻ 0.01) compared with controls. GSIS during the NE infusion was also reduced (P Ͻ 0.05) compared with pretreatment values. GSIS and GPAIS were approximately fourfold greater (P Ͻ 0.01) in NE fetuses 3 h after the 7 days that NE infusion was discontinued compared with age-matched controls or pretreatment GSIS and GPAIS values of NE fetuses. In isolated pancreatic islets from NE fetuses, mRNA concentrations of adrenergic receptor isoforms (␣1D, ␣2A, ␣2C, and ␤1), G protein subunit-␣i-2, and uncoupling protein 2 were lower (P Ͻ 0.05) compared with controls, but ␤-cell regulatory genes were not different. Our findings indicate that chronic exposure to elevated NE persistently suppresses insulin secretion. After removal, NE fetuses demonstrated a compensatory enhancement in insulin secretion that was associated with adrenergic desensitization and greater stimulus-secretion coupling in pancreatic islets. adrenergic receptor; ␤-cell; intrauterine growth restriction; uncoupling protein 2; catecholamines SMALL-FOR-GESTATIONAL AGE or intrauterine growth-restricted (IUGR) infants are at greater risk for developing metabolic diseases such as type 2 diabetes mellitus (29,40,54). Impaired insulin secretion is associated with a diabetic phenotype indicating that in utero complications can permanently compromise ␤-cell development and function (27,28). A fetal sheep model with placental insufficiency-induced intruterine growth restriction shares many similarities with human IUGR fetuses, such as asymmetric growth, hypoxemia, hypoglycemia, hypoinsulinemia, and hypercatecholaminemia [epinephrine and norepinephrine (NE)] (4, 16,18,22,23,32,41,47). Furthermore, glucose-stimulated insulin secretion (GSIS) and ␤-cell mass are lower in IUGR sheep fetuses, which also replicate features in human IUGR fetuses (34 -36, 41, 53). Several characteristics of the fetal IUGR environment, including hypoglycemia, hypoxemia, and hypercatecholaminemia, are proposed to ...

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Amniotic fluid catecholamines and metabolites in intrauterine growth retardation

Cited by 26 publications

References 17 publications

Amniotic Fluid Norepinephrine Concentration as an Indicator of Fetal Sympathetic Nervous Activity

Amniotic Fluid Norepinephrine Concentration as an Indicator of Fetal Sympathetic Nervous Activity

Intrauterine Growth Retardation and Fetal Cardiac Function

Enhanced insulin secretion responsiveness and islet adrenergic desensitization after chronic norepinephrine suppression is discontinued in fetal sheep

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