Composition and Volume of Fluid Swallowed by Fetal Sheep

Harding, Richard; Bocking, AD; Sigger, J. N.; Wickham, P. J. D.

doi:10.1113/expphysiol.1984.sp002835

Cited by 78 publications

(28 citation statements)

References 16 publications

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“…Assuming amniotic fluid IGF-I concentrations of 2·5 ng/ml and fetal swallowing rate increasing from 200 ml/day at 90 days to 800 ml/day in late gestation (Harding et al 1984, Tomoda et al 1985, this would equate to the fetus swallowing IGF-I from amniotic fluid at a rate of 0·5 µg/day at 90 days increasing to 2 µg/day at term. However, swallowed fluid not only consists of amniotic fluid but also of pulmonary fluid and naso-oral secretions, both of which contain high levels of IGF-I (Schindler 1982, Hill et al 1984.…”

Section: Discussionmentioning

confidence: 99%

“…It has been estimated that the human fetus swallows up to 760 ml amniotic fluid per day in late gestation (Pritchard 1965, Gitlin et al 1972, and the ovine fetus up to 2000 ml per day (Harding et al 1984, Tomoda et al 1985. Amniotic fluid contains proteins, carbohydrates and growth factors such as insulin-like growth factor-I (IGF-I) and epidermal growth factor (EGF) (Schindler 1982, Merimee et al 1984, Weaver et al 1990).…”

Section: Introductionmentioning

confidence: 99%

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Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Kimble¹,

Breier²,

Gluckman³

et al. 1999

Journal of Endocrinology

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Infants with upper gut atresia often have impaired intrauterine growth and gut function. IGF-I is important in fetal growth and is contained in amniotic fluid. We therefore wanted to test the hypothesis that IGF-I infused into fetal gut would reverse the effects of an upper gut obstruction on gut structure and growth in fetal sheep.At 90 days gestation fetuses (n=6 per group) underwent oesophageal ligation, followed by continuous infusion of IGF-I (1-8 µg/day) or saline into the gut beyond the ligation until 137 days. Controls underwent sham ligation only. Oesophageal ligation tended to reduce fetal body and organ weights. IGF-I treatment prevented this reduction and increased body length and spleen weight above those of controls. The decrease in bowel wall thickness induced by oesophageal ligation was also prevented by IGF-I treatment. Amniotic fluid IGF-I concentrations did not change over gestation and were higher in the IGF-I treated group. No change in fetal plasma IGF-I concentrations were detectable. We conclude that enterally administered IGF-I may enhance fetal growth and gut development in utero and that IGF-I in amniotic fluid may play a physiological role in gut development in the fetus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Kimble¹,

Breier²,

Gluckman³

et al. 1999

Journal of Endocrinology

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“…The fetus is bathed in amniotic fluid throughout gestation. During pregnancy, to further the development of fetal respiratory and digestive systems, the fetus recirculates amniotic fluid (up to 500 ml/day) via oronasal ingestion (73)(74)(75)(76). Amniotic fluid consists of maternal plasma and fetal urine, depending upon gestational stage (77)(78)(79).…”

Section: Discussionmentioning

confidence: 99%

Infectious Prions in the Pregnancy Microenvironment of Chronic Wasting Disease-Infected Reeves' Muntjac Deer

Nalls

McNulty

Hoover

et al. 2017

J Virol

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Ample evidence exists for the presence of infectious agents at the maternal-fetal interface, often with grave outcomes to the developing fetus (i.e., Zika virus, brucella, cytomegalovirus, and toxoplasma). While less studied, pregnancyrelated transmissible spongiform encephalopathies (TSEs) have been implicated in several species, including humans. Our previous work has shown that prions can be transferred from mother to offspring, resulting in the development of clinical TSE disease in offspring born to muntjac dams infected with chronic wasting disease (CWD) (1). We further demonstrated protein misfolding cyclic amplification (PMCA)-competent prions within the female reproductive tract and in fetal tissues harvested from CWD experimentally and naturally exposed cervids (1, 2). To assess whether the PMCA-competent prions residing at the maternal-fetal interface were infectious and to determine if the real-time quaking-induced conversion (RT-QuIC) methodology may enhance our ability to detect amyloid fibrils within the pregnancy microenvironment, we employed a mouse bioassay and RT-QuIC. In this study, we have demonstrated RT-QuIC seeding activity in uterus, placentome, ovary, and amniotic fluid but not in allantoic fluids harvested from CWD-infected Reeves' muntjac dams showing clinical signs of infection (clinically CWD-infected) and in some placentomes from pre-clinically CWD-infected dams. Prion infectivity was confirmed within the uterus, amniotic fluid, and the placentome, the semipermeable interface that sustains the developing fetus, of CWD-infected dams. This is the first report of prion infectivity within the cervid pregnancy microenvironment, revealing a source of fetal CWD exposure prior to the birthing process, maternal grooming, or encounters with contaminated environments.IMPORTANCE The facile dissemination of chronic wasting disease within captive and free-range cervid populations has led to questions regarding the transmission dynamics of this disease. Direct contact with infected animals and indirect contact with infectious prions in bodily fluids and contaminated environments are suspected to explain the majority of this transmission. A third mode of transmission, from mother to offspring, may be underappreciated. The presence of pregnancyrelated prion infectivity within the uterus, amniotic fluid, and the placental structure reveals that the developing fetus is exposed to a source of prions long before exposure to the infectious agent during and after the birthing process or via contact with contaminated environments. These findings have impact on our current concept of CWD disease transmission.KEYWORDS CWD, maternal, pregnancy, prions T ransmissible spongiform encephalopathies (TSEs), or prion diseases, are proteinaceous infectious neurodegenerative diseases affecting animals, including humans (3, 4). The disease is caused by the accumulation of an aberrant misfolded form

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“…The close relationship between fetal plasma and amniotic fluid levels in the present study points to the fetus as the source of these proteins. It seems likely that they are contained in fetal urine, tracheal and oronasopharyngeal secretions, which have been shown to contain IGF-I and epidermal growth factor and contribute significantly to the daily amniotic fluid production (Harding et al 1984, Trahair & Harding 1994. Alternatively, transmembraneous transport or even an extra-fetal source cannot be entirely ruled out, as there are data that show that the placenta might regulate fetal IGFs (Bassett et al 1990, Iwamoto et al 1992.…”

Section: Igf-i Concentrations In the Fetusmentioning

confidence: 99%

Chronic pulsatile infusion of growth hormone to growth-restricted fetal sheep increases circulating fetal insulin-like growth factor-I levels but not fetal growth

Bauer

Breier²,

Bloomfield³

et al. 2003

Journal of Endocrinology

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Intra-uterine growth restriction (IUGR) is a major cause of perinatal mortality and morbidity. Postnatally, growth hormone (GH) increases growth, increases circulating insulin-like growth factor (IGF)-I levels, and alters metabolism. Our aim was to determine if GH infusion to IUGR fetal sheep would alter fetal growth and metabolism, and thus provide a potential intra-uterine treatment for the IUGR fetus.We studied three groups of fetuses: control, IUGR+ vehicle and IUGR+GH (n=5 all groups). IUGR was induced by repeated embolisation of the placental vascular bed between 110 and 116 days of gestation (term=145 days). GH (3·5 mg/kg/day) or vehicle was infused in a pulsatile manner from 117 to 127 days of gestation.Embolisation reduced fetal growth rate by 25% (P<0·01) and reduced the weight of the fetal liver (20%), kidney (23%) and thymus (31%; all P<0·05). GH treatment further reduced the weight of the fetal kidneys (32%) and small intestine (35%; both P<0·04), but restored the relative weight of the fetal thymus and liver (P<0·05). Embolisation decreased fetal plasma IGF-I concentrations (48%, P<0·001) and increased IGF binding protein 1 (IGFBP-1) concentrations (737%, P<0·002). GH treatment restored fetal plasma IGF-I concentrations to control levels, while levels in IUGR+vehicle fetuses stayed low (P<0·05 vs control). IGFBP-1 and IGFBP-2 concentrations were about sevenfold lower in amniotic fluid than in fetal plasma, but amniotic and plasma concentrations were closely correlated (r=0·75, P<0·0001 and r=0·55 P<0·0001 respectively). Embolisation transiently decreased fetal blood oxygen content (40%, P<0·002), and increased blood lactate concentrations (213%, P<0·04). Both returned to pre-embolisation levels after embolisation stopped, but blood glucose concentrations declined steadily in IUGR+vehicle fetuses. GH treatment maintained fetal blood glucose concentrations at control levels.Our study shows that GH infusion to the IUGR fetal sheep restores fetal IGF-I levels but does not improve fetal growth, and further reduces the fetal kidney and intestine weights. Thus, fetal GH therapy does not seem a promising treatment stratagem for the IUGR fetus.

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Composition and Volume of Fluid Swallowed by Fetal Sheep

Cited by 78 publications

References 16 publications

Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Infectious Prions in the Pregnancy Microenvironment of Chronic Wasting Disease-Infected Reeves' Muntjac Deer

Chronic pulsatile infusion of growth hormone to growth-restricted fetal sheep increases circulating fetal insulin-like growth factor-I levels but not fetal growth

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