Cited by 35Pregnancy and preeclampsia studiesNeonatal and fetal brain pathologyBirth, Development, and Health

Oxygen, glucose, and lactate uptake by fetus and placenta during prolonged hypoxemia

Hooper, S. B., Walker, D. W., Harding, R.·1995·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

Abstract

Our aim was to compare the effects of short (4 h) and prolonged (24 h) periods of reduced uterine blood flow (RUBF) on fetal and placental uptake of O2, glucose, and lactate. In pregnant sheep, uterine and umbilical blood flows were measured under normal conditions and after 4 and 24 h of RUBF. A 50% reduction in uterine blood flow caused a 56% reduction in fetal arterial O2 saturation (SaO2). Umbilical blood flow increased from 325 +/- 33 to 378 +/- 32 ml.min-1.kg-1 (P < 0.05) after 4 h but was not different from pre-RUBF values after 24 h. O2 uptake by the gravid uterus was not altered by RUBF, due to an increase (84%) in uterine O2 extraction. Similarly, uteroplacental and fetal O2 consumptions and fetal glucose uptake were not affected by RUBF, whereas uteroplacental glucose uptake was significantly reduced after 4 h (by 42%) and 24 h (by 58%) of RUBF. Fetal lactate uptake was greatly reduced from 78.7 +/- 15.5 to -167 +/- 57 mumol.min-1.kg-1 after 4 h and to -198 +/- 80 mumol.min-1.kg-1 after 24 h of RUBF; negative values indicate placental lactate uptake from the fetal circulation. Thus, although RUBF significantly reduced fetal SaO2, fetal and uteroplacental O2 consumptions did not change. In addition, although fetal glucose uptake was not altered by RUBF, during RUBF the placenta became a major site of lactate clearance from the fetal circulation.

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Crossref · 10.1152/ajpregu.1995.268.2.r303

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  • In sheep, fetal oxygen consumption is maintained when fetal-placental hypoxia is induced by restricting uterine blood flow and, hence, uterine oxygen delivery for 24h.

    “Similarly, in sheep, fetal oxygen consumption is maintained when fetal-placental hypoxia is induced by restricting uterine blood flow and, hence, uterine oxygen delivery for 24h (53, 263).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [263]

  • Lactate production by ovine uteroplacental tissues is reduced by 24 h of placental-fetal hypoxemia induced by restricting uterine blood flow or placental growth by hyperthermia.

    “Certainly, lactate production by ovine uteroplacental tissues is reduced by 24 h of placental-fetal hypoxemia induced by restricting uterine blood flow or placental growth by hyperthermia (263, 456).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [263]

  • With shorter episodes of severe hypoxia (<48h) in pregnant sheep, there is evidence for activation of fetal glucogenesis and increased delivery of glucose and lactate to the placenta from the fetal circulation.

    “With shorter episodes of severe hypoxia (<48h) in pregnant sheep, there is evidence for activation of fetal glucogenesis and increased delivery of glucose and lactate to the placenta from the fetal circulation (230, 263, 292).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [263]

  • In contrast to oxygen, the ovine placenta appears to spare glucose for onward passage to the fetus during acute hypoxemia as fetal glucose delivery and consumption are maintained at the expense of utero-placental glucose consumption for periods of up to 24h.

    “In contrast to oxygen, the ovine placenta appears to spare glucose for onward passage to the fetus during acute hypoxemia as fetal glucose delivery and consumption are maintained at the expense of utero-placental glucose consumption for periods of up to 24h (53,230,263,380,525).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [263]

  • Consequently, there is little evidence for placental oxygen sparing in response to acute normobaric hypoxia in sheep, as may occur in the human placenta in response to the chronic hypoxia of high altitude.

    “Consequently, there is little evidence for placental oxygen sparing in response to acute normobaric hypoxia in the sheep (230, 263, 380), as may occur in the human placenta in response to the chronic hypoxia of high altitude (271).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [263]

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Authors
Hooper, S. B., Walker, D. W., & Harding, R.
Affiliations
Monash University (AU)
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Published
1995-02-01
Volume
268
Issue
2
Pages
R303-R309
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
OpenAlex
W2338436696
Cited by
35
References
0
Citations by year
2025: 1 · 2021: 2 · 2020: 2 · 2019: 2 · 2017: 1 · 2016: 3 · 2015: 2 · 2013: 1 · 2012: 2
FWCI
1.60
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Keywords
fetal hypoxemia, lactate clearance, umbilical blood flow, pregnant sheep
MeSH terms
Animals, Hypoxia, Arteries, Female, Fetal Blood, Fetus, Gases, Glucose, Hydrogen-Ion Concentration, Lactates, Oxygen, Oxygen Consumption, Placenta, Pregnancy, Regional Blood Flow, Sheep, Time Factors, Uterus, Lactic Acid

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