Fetal Response to Intrauterine Stress

Thornburg, Kent L.

doi:10.1002/9780470514047.ch3

Cited by 18 publications

(5 citation statements)

References 29 publications

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“…Consistent with this is an observation of better Apgar scores in neonates of women with greater negative emotionality during pregnancy (Ponirakis et al, 1998). The fetus responds to hypoxic threats, such as cord compression or maternal hypoxia, by increasing the volume of blood directed to the brain, heart, and adrenals above that of nonstress conditions (Thornburg, 1991). Supportive, although indirect, evidence of the beneficial effects of mild physiological stress can be found in a series of studies comparing matched groups of women who either continued to exercise during pregnancy or refrained from training.…”

Section: Discussionmentioning

confidence: 99%

Maternal Psychological Distress During Pregnancy in Relation to Child Development at Age Two

et al. 2006

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Concern exists that a constellation of negative maternal emotions during pregnancy generates persistent negative consequences for child development. Maternal reports of anxiety, pregnancy-specific and nonspecific stress, and depressive symptoms were collected during mid-pregnancy and at 6 weeks and 24 months after birth in a sample of healthy women with low risk pregnancies. Developmental assessment and cardiac vagal tone monitoring were administered to 94 children at age 2. Higher levels of prenatal anxiety, nonspecific stress, and depressive symptoms were associated with more advanced motor development in children after postnatal control for each psychological measure; anxiety and depression were also significantly and positively associated with mental development. Mild to moderate levels of psychological distress may enhance fetal maturation in healthy populations.

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Section: Discussionmentioning

confidence: 99%

Maternal Psychological Distress During Pregnancy in Relation to Child Development at Age Two

et al. 2006

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“…In humans, changes in fetal heart rate have long been observed in fetuses in response to intrauterine stress [104]. Animal studies have also confirmed the dysfunction of the myocardium in response to hypoxia.…”

Section: Fetal Hypoxia and Abnormal Heart Developmentmentioning

confidence: 99%

Hypoxia and Fetal Heart Development

Patterson¹,

Zhang²

2010

CMM

202

151

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Fetal hearts show a remarkable ability to develop under hypoxic conditions. The metabolic flexibility of fetal hearts allows sustained development under low oxygen conditions. In fact, hypoxia is critical for proper myocardial formation. Particularly, hypoxia inducible factor 1 (HIF-1) and vascular endothelial growth factor play central roles in hypoxia-dependent signaling in fetal heart formation, impacting embryonic outflow track remodeling and coronary vessel growth. Although HIF is not the only gene involved in adaptation to hypoxia, its role places it as a central figure in orchestrating events needed for adaptation to hypoxic stress. Although "normal" hypoxia (lower oxygen tension in the fetus as compared with the adult) is essential in heart formation, further abnormal hypoxia in utero adversely affects cardiogenesis. Prenatal hypoxia alters myocardial structure and causes a decline in cardiac performance. Not only are the effects of hypoxia apparent during the perinatal period, but prolonged hypoxia in utero also causes fetal programming of abnormality in the heart's development. The altered expression pattern of cardioprotective genes such as protein kinase c epsilon, heat shock protein 70, and endothelial nitric oxide synthase, likely predispose the developing heart to increased vulnerability to ischemia and reperfusion injury later in life. The events underlying the long-term changes in gene expression are not clear, but likely involve variation in epigenetic regulation.

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“…It has been previously established that growth restriction successfully balances reduced oxygen delivery and consumption. Chronic hypoxia in IUGR causes fetal circulatory redistribution during gestation to cardinal organs (brain, myocardium, and adrenal glands), 31 the ''brain-sparing'' effect, which is a fetal adaptive reaction to placental insufficiency. Fetal liver receives approximately 70-75% of the blood from the nutrient-and oxygen-rich umbilical venous (UV) blood, and shunting UV blood through the ductus venosus (DV), thereby bypassing the liver and delivering nutrientrich blood to the systemic circulation, is one mechanism of redistributing cardiac output, which contributes to the brain sparing seen in IUGR fetuses and results in reduced adaptation and function of the liver.…”

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confidence: 99%

Intraplacental Gene Therapy with Ad-IGF-1 Corrects Naturally Occurring Rabbit Model of Intrauterine Growth Restriction

et al. 2015

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Intrauterine growth restriction (IUGR) due to placental insufficiency is a leading cause of perinatal complications for which there is no effective prenatal therapy. We have previously demonstrated that intraplacental injection of adenovirus-mediated insulin-like growth factor-1 (Ad-IGF-1) corrects fetal weight in a murine IUGR model induced by mesenteric uterine artery branch ligation. This study investigated the effect of intraplacental Ad-IGF-1 gene therapy in a rabbit model of naturally occurring IUGR (runt) due to placental insufficiency, which is similar to the human IUGR condition with onset in the early third trimester, brain sparing, and a reduction in liver weight. Laparotomy was performed on New Zealand White rabbits on day 21 of 30 days of gestation and litters were divided into five groups: Control (first position) + phosphate-buffered saline (PBS), control + Ad-IGF-1, runt (third position) + PBS, runt + Ad-IGF-1, and runt + Ad-LacZ. The effect of IGF-1 gene therapy on fetal, placental, liver, heart, lung, and musculoskeletal weights of the growthrestricted pups was examined. Protein expression after gene transfer was seen along the maternal-fetal placenta interface (n = 12) 48 hr after gene therapy. There was minimal gene transfer detected in the pups or maternal organs. At term, compared with the normally grown first-position control, the runted third-position pups demonstrated significantly lower fetal, placental, liver, lung, and musculoskeletal weights. The fetal, liver, and musculoskeletal weights were restored to normal by intraplacental Ad-IGF-1 gene therapy ( p < 0.01), with no change in the placental weight. Intraplacental gene therapy is a novel strategy for the treatment of IUGR caused by placental insufficiency that takes advantage of an organ that will be discarded at birth. Development of nonviral IGF-1 gene delivery using placenta-specific promoters can potentially minimize toxicity to the mother and fetus and facilitate clinical translation of this novel therapy.

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Fetal Response to Intrauterine Stress

Cited by 18 publications

References 29 publications

Maternal Psychological Distress During Pregnancy in Relation to Child Development at Age Two

Maternal Psychological Distress During Pregnancy in Relation to Child Development at Age Two

Hypoxia and Fetal Heart Development

Intraplacental Gene Therapy with Ad-IGF-1 Corrects Naturally Occurring Rabbit Model of Intrauterine Growth Restriction

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