The role of amniotic fluid in influencing neonatal birth weight

Burjonrappa, Sathyaprasad; Crete, Elise; Bouchard, Sarah

doi:10.1038/jp.2009.102

Cited by 21 publications

(13 citation statements)

References 8 publications

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“…In this model, complete intestinal obstruction is induced prenatally, resulting in dilation of the upstream segment and narrowing of the downstream segment, as observed in other experimental models and in human prenatal atresia [11], [13], [22]. Like in human neonates, rat pups with intestinal atresia had a low birth weight, partly attributed to the lack of amniotic fluid circulation and absorption in the distal intestine [23], [24]. One noteworthy difference between the experimental model and the clinical setting is the duration of the obstruction.…”

Section: Discussionmentioning

confidence: 79%

Prenatal Intestinal Obstruction Affects the Myenteric Plexus and Causes Functional Bowel Impairment in Fetal Rat Experimental Model of Intestinal Atresia

et al. 2013

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BackgroundIntestinal atresia is a rare congenital disorder with an incidence of 3/10 000 birth. About one-third of patients have severe intestinal dysfunction after surgical repair. We examined whether prenatal gastrointestinal obstruction might effect on the myenteric plexus and account for subsequent functional disorders.Methodology/Principal FindingsWe studied a rat model of surgically induced antenatal atresia, comparing intestinal samples from both sides of the obstruction and with healthy rat pups controls. Whole-mount preparations of the myenteric plexus were stained for choline acetyltransferase (ChAT) and nitric oxide synthase (nNOS). Quantitative reverse transcription PCR was used to analyze mRNAs for inflammatory markers. Functional motility and permeability analyses were performed in vitro. Phenotypic studies were also performed in 8 newborns with intestinal atresia. In the experimental model, the proportion of nNOS-immunoreactive neurons was similar in proximal and distal segments (6.7±4.6% vs 5.6±4.2%, p = 0.25), but proximal segments contained a higher proportion of ChAT-immunoreactive neurons (13.2±6.2% vs 7.5±4.3%, p = 0.005). Phenotypic changes were associated with a 100-fold lower concentration-dependent contractile response to carbachol and a 1.6-fold higher EFS-induced contractile response in proximal compared to distal segments. Transcellular (p = 0.002) but not paracellular permeability was increased. Comparison with controls showed that modifications involved not only proximal but also distal segments. Phenotypic studies in human atresia confirmed the changes in ChAT expression.ConclusionExperimental atresia in fetal rat induces differential myenteric plexus phenotypical as well as functional changes (motility and permeability) between the two sides of the obstruction. Delineating these changes might help to identify markers predictive of motility dysfunction and to define guidelines for post-surgical care.

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Section: Discussionmentioning

confidence: 79%

Prenatal Intestinal Obstruction Affects the Myenteric Plexus and Causes Functional Bowel Impairment in Fetal Rat Experimental Model of Intestinal Atresia

et al. 2013

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“…47,48 The deflection of intra-uterine growth is usually detected at the end of the second trimester or beginning of the third, when the fetus begins actively to swallow the amniotic fluid, which is thought to partially contribute to fetal growth. 49 The fetus with gastroschisis is, indeed, in a condition of intestinal subocclusion due to both herniation of loops, which can be variously damaged, and their constriction at the level of the defect. The result is a reduced assumption and absorption of nutrients from the amniotic fluid.…”

Section: Prenatal Diagnosis and Management Of Pregnancymentioning

confidence: 99%

Abdominal wall defects: Prenatal diagnosis, newborn management, and long-term outcomes

Gamba¹,

Midrio²

2014

Seminars in Pediatric Surgery

130

108

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“…2 Animal studies and limited human observations suggest that swallowed amniotic fluid accounts for about 15% of fetal growth. 3–5 …”

Section: Amniotic Fluid “Premature” Human Milk and “Term” Human Milkmentioning

confidence: 99%

Human Milk for the Premature Infant

Underwood

2013

Pediatric Clinics of North America

341

237

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Synopsis Premature infants are a heterogeneous group with widely differing needs for nutrition and immune protection with risk of growth failure, developmental delays, necrotizing enterocolitis, and late-onset sepsis increasing with decreasing gestational age and birth weight. Human milk from women delivering prematurely has more protein and higher levels of many bioactive molecules compared to milk from women delivering at term. Human milk must be fortified for small premature infants to achieve adequate growth. Mother’s own milk improves growth and neurodevelopment and decreases the risk of necrotizing enterocolitis and late-onset sepsis and should therefore be the primary enteral diet of premature infants. Donor milk is a valuable resource for premature infants whose mothers are unable to provide an adequate supply of milk, but presents significant challenges including the need for pasteurization, nutritional and biochemical deficiencies and a limited supply.

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The role of amniotic fluid in influencing neonatal birth weight

Cited by 21 publications

References 8 publications

Prenatal Intestinal Obstruction Affects the Myenteric Plexus and Causes Functional Bowel Impairment in Fetal Rat Experimental Model of Intestinal Atresia

Prenatal Intestinal Obstruction Affects the Myenteric Plexus and Causes Functional Bowel Impairment in Fetal Rat Experimental Model of Intestinal Atresia

Abdominal wall defects: Prenatal diagnosis, newborn management, and long-term outcomes

Human Milk for the Premature Infant

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