Intrauterine Growth Retardation: Pathophysiology and Possibilities for Intrauterine Treatment

Johnson, Mark P.; Evans, Mark I.

doi:10.1159/000263292

Cited by 15 publications

(5 citation statements)

References 33 publications

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“…Fetal malnutrition and hypoxia, caused by either an insufficient nutrient and oxygen delivery via reduced uteroplacental perfusion or improper transport of nutrients and oxygen across the maternal placental barrier limits fetal growth 8,9 and results in an increased risk for development of hypertension and cardiovascular disease. 3,10 -12,25,28 We recently reported that placental insufficiency initiated at day 14 of the 22-day gestational period in the pregnant rat results in growthrestricted offspring predisposed to the development of hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…4 -7 Fetal malnutrition limits fetal growth and results in small-for-gestational-age newborns. 8,9 Findings from both epidemiological and animal studies suggest that fetal malnutrition may also program or permanently alter fetal structure and physiology, resulting in an increased risk for development of hypertension and cardiovascular disease. 3,10 -12 However, the mechanisms mediating low birth weight (LBW) and hypertension remain to be elucidated.…”

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confidence: 99%

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Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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Abstract-Low birth weight is a risk factor for the subsequent development of hypertension in humans. We previously reported that reduced uterine perfusion in the pregnant rat results in growth-restricted offspring predisposed to the development of hypertension. The purpose of this study was to determine whether the sympathetic nervous system plays a role in mediating hypertension in this model of low birth weight. Key Words: hypertension, pregnancy Ⅲ rats Ⅲ renal nerves Ⅲ denervation Ⅲ sympathetic nervous system H ypertension is a multifactorial disorder thought to result from both genetic and environmental factor interactions. Recent epidemiological studies 1,2 suggest that a predisposition for development of hypertension may be programmed by factors initiated in utero, 3 an observation supported by many animal studies. 4 -7 Fetal malnutrition limits fetal growth and results in small-for-gestational-age newborns. 8,9 Findings from both epidemiological and animal studies suggest that fetal malnutrition may also program or permanently alter fetal structure and physiology, resulting in an increased risk for development of hypertension and cardiovascular disease. 3,10 -12 However, the mechanisms mediating low birth weight (LBW) and hypertension remain to be elucidated.In humans, few studies have examined the relationship between the sympathetic nervous system (SNS) and LBW, and controversy exists with regards to whether LBW individuals are associated with increases [13][14][15] or decreases in sympathetic activity. 16 Evidence for alterations in the SNS is noted in some animal models of intrauterine growth restriction (IUGR), because plasma levels of circulating catecholamines are increased. [17][18][19][20][21] This observation has been noted in growth-restricted offspring from pregnant rats fed a proteinrestricted diet during gestation, 17 in a naturally occurring model of IUGR using piglets, 18,19 and in a model of IUGR induced by placental insufficiency in the rat 20 and in sheep. 21 Additionally, hypoxia during fetal development leads to increased sympathetic innervation. 22,23 However, no further assessment of the SNS in association with IUGR has been examined.Nutrient and oxygen supply limitations are the components of the intrauterine environment that limit fetal growth and result in small-for-gestational-age newborns. Because IUGR within the Western world is more likely the result of reduced uterine perfusion, 24 we have developed a model of fetal programming induced by placental insufficiency caused by hypoxia and fetal undernutrition. 25 Using this model, we previously reported that reduced uterine perfusion initiated at day 14 of gestation in the rat results in growth-restricted offspring that are hypertensive as early as 4 weeks of age. 25 Furthermore, marked elevations in mean arterial pressure (MAP) remain evident in male growth-restricted offspring at 12 weeks of age. Because increased renal sympathetic nerve activity appears to be a causal mechanism in primary hypertension, 26 we determined the ro...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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“…If generalized symmetric (type-I) IUGR were present, then no organ sparing should be present, and the predicted visceral weights for body-based and brain-based calculations should be similar. If values are dissimilar between body-and brain-based calculations, then asymmetrical (type-II) IUGR is suggested; the basis of these differences may originate from a higher than expected brain weight resulting from a 'type-II' brain-sparing effect [1],…”

Section: Methodsmentioning

confidence: 99%

“…Genetic imbalances, initiated at the time of conception, are thought to lead to a generalized reduction in growth potential manifested as symmetrical (type-I) IUGR [1], While there are reason able data on fetal and organ weights at term, investigation into midgestational growth re pression has been hampered by a lack of precise reference standards against which to compare observed fetal body and organ weights. Tables of body and organ weights based on autopsies of normal fetuses at var ious gestational ages are available; the most widely referenced is that of Gruenwald and Minh [2], Unfortunately, such tables are based on gestational age from the last men strual period (LMP) with its inherent impre cision [3][4][5], fetal body weight rounded off to 250-gram increments, and standard devia tions of normal values ranging up to 50% of the mean or more.…”

Section: Introductionmentioning

confidence: 99%

Symmetrical Intrauterine Growth Retardation Is Not Symmetrical: Organ-Specific Gravimetric Deficits in Midtrimester and Neonatal Trisomy 18

Johnson

Barr²,

Qureshi³

et al. 1989

Fetal Diagn Ther

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Models to predict normal fetal growth have been of limited accuracy. Abnormal growth is even more problematic. We have developed a mathematical modeling system based on observed body and brain weights to study fetal growth patterns in midgestational trisomy 18 fetuses. Third-degree polynomial-based analysis using observed fetal body and brain weights to generate predicted weights for various organ systems allows for the comparative study of growth patterns at various fetal weights and gestational ages. Our data suggest that what has been previously called symmetrical intrauterine growth retardation associated with aneuploid fetuses is really an asymmetrical pattern that is dynamic in nature and may change through the course of pregnancy.

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“…Disrupt growth and function of fetus β-cell, result less secretion of insulin, a mechanism of insulin resistance in malnourished fetus (Blondeau et al, 2001). Recent research show evidence that susceptibility for the development of HTN can be lay out by pre-birth aspects Fetus growth retardation and premature baby birth is due to fetus undernourishment (Johnson and Evans, 1987;Bernstein et al, 2002). There is increase chances for the onset of HTN and CVD in undernourished fetus because nutrients restriction alter the structure and function of fetus organs, it is proposed by both epidemiological and animal model research (Woods, 2000;Holemans et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Metabolic Syndrome Development in Relation to Low Birth Weight

Arif¹,

Tahira²,

Abbas³

et al. 2014

JGIASS

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The metabolic syndromes are constellation of major risk factor for high fasting tri-aceylglycerols, obesity, low level of HDL cholesterol, higher fasting plasma insulin, hypertension and impaired glucose tolerance. A rat model of maternal diet was used to observe this relationship. This study investigated the metabolic syndrome development in relation to low birth weight. In this study 4 pairs of rats was used and was divided into 2 groups each consisting of 2 pairs as G1 normal and G2 was taken from animal lab of national institute of food science and technology. Control group was fed standard diet. Experimental group was fed 50% low diet as compared to control group during child bearing and lactation period. Offspring of rats was introduced solid diet and then reviewed at 20 day and 40 day of age respectively. The mother body weight and feed intake was measured daily. The overall mean body weight of mothers was significantly increased in control and decreased in experimental group. The control dam's offspring body weight significantly higher than experimental dam's offspring till weaning, however low birth weight offspring of rats show catch-up growth after weaning or 20 days. Serum glucose, cholesterol level of low birth weight offspring of rat's was higher than normal weight offspring.

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Intrauterine Growth Retardation: Pathophysiology and Possibilities for Intrauterine Treatment

Cited by 15 publications

References 33 publications

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

Symmetrical Intrauterine Growth Retardation Is Not Symmetrical: Organ-Specific Gravimetric Deficits in Midtrimester and Neonatal Trisomy 18

Metabolic Syndrome Development in Relation to Low Birth Weight

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