Effective uterine blood flow during labor

Wright, Helen Payling; Morris, Norman; Osborn, S. B.; Hart, A.

doi:10.1016/0002-9378(58)90542-8

Cited by 29 publications

(2 citation statements)

References 16 publications

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“…Thus the consequences of, and physiological causes of reduction in maternal placental blood flow, and particularly the effects of the ensuing hypoxia, have been the subject of intensive investigation (Cohn, Sacks, Heyman, & Rudolph, 1974;Boddy, Dawes, Fisher, Pinter & Robinson, 1974;Jones & Robinson, 1975;Robinson, Jones & Thorburn, 1977;Jansen, Krane, Thomas, Beck, Lowe, Joyce, Parr & Nathanielsz, 1979;Peeters, Sheldon, Jones, Makowski & Meschia, 1979;Parer, Krueger & Harris, 1980;Harding, Poore & Cohen, 1981; Goetzman & Rudolph, 1982). For instance, acute reduction in uterine blood flow associated with uterine contraction was first reported in the dog by Ahlquist & Woodbury (1947) and subsequently observed, together with the associated fetal hypoxia, by many others (Assali, Dasgupta, Kolin & Holm, 1958;Wright, Morris, Osborn & Hart, 1958;Ramsey, 1968; Huch, Huch, Schneider & Rooth, 1977;Jensen & Kunzel, 1980;Harding, Sigger & Wickham, 1983). Such observations, and those on the effects of experimentally induced reduction of uterine blood flow for short periods, imply that the fetal circulation in the short-term is re-adjusted to maintain blood and nutrient supply to the heart and head (Peeters et al 1979;Parer et al 1980;Harding et al 1981;Itskovitz et al 1982; Kunzel, Kastendieck & Hohmann, 1983), but they say little about the mechanisms of many of the responses or about the associated placental-fetal interactions.…”

Section: Introductionmentioning

confidence: 99%

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Gu¹,

Jones²,

Parer³

1985

The Journal of Physiology

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SUMMARY1. The effects on the fetus and placenta of graded reductions of uterine blood flow to 30-90 % of control have been studied in sheep at days 125-143 of pregnancy.2. Reduction of uterine flow to 70-90 % of control had little effect upon fetal oxygenation or heart rate or blood pressure but elevated fetal plasma catecholamine concentration.3. Reduction of flow to 30-50 % of control depressed fetal arterial and umbilical venous Po2 but had little effect upon oxygen consumption unless the umbilical venous value fell below about 14 mmHg when it was depressed by up to 30 %. Placental oxygen consumption did not fall and was therefore maintained at the expense of the fetus. Fetal arterial pressure rose by 10-12 mmHg and heart rate fell by about 30 beats/min during the first 10-15 min then rose above its initial value. Plasma adrenaline and noradrenaline concentrations rose progressively at a rate which increased with greater degrees of asphyxia. 4. When uterine blood flow was reduced below one-half of normal, net placental consumption of glucose fell and there was evidence of substantial provision of glucose and lactate from the fetus. Fetal production of lactate increased sharply and much of this appeared to be consumed by the placenta at a rate sufficient to account entirely for the deficit in net glucose consumption. 5. The results are consistent with the hypothesis that the fetus senses even small changes in uterine blood flow that are alone insufficient to elicit significant blood gas changes. When the fall in uterine flow caused by arterial compression is relatively large, nutrient supply to the placenta is maintained at the expense of the fetus and as a result of fetal glucose and lactate production. The elevation of fetal arterial Pco, appears to enhance fetal responses to hypoxia. The results are discussed in relation to the fetal responses to brief and prolonged reductions in uterine blood flow.

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Section: Introductionmentioning

confidence: 99%

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Gu¹,

Jones²,

Parer³

1985

The Journal of Physiology

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“…Most cases of fetal distress during labor can be attributed to inadequate placental perfusion or preexisting placental deterioration that impairs metabolic exchange with the fetus [ 96 ]. During contractions, the uterine blood flow can drop by more than half, which may result in intrapartum fetal compromise [ 97 ]. When fetal distress is evidenced, emergency operative delivery is the therapeutic option.…”

Section: Fetal Distressmentioning

confidence: 99%

Sildenafil during the 2nd and 3rd Trimester of Pregnancy: Trials and Tribulations

Bie

Basurto

Kumar

et al. 2022

IJERPH

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Sildenafil, a phosphodiesterase 5 inhibitor with a vasodilatory and anti-remodeling effect, has been investigated concerning various conditions during pregnancy. Per indication, we herein review the rationale and the most relevant experimental and clinical studies, including systematic reviews and meta-analyses, when available. Indications for using sildenafil during the second and third trimester of pregnancy include maternal pulmonary hypertension, preeclampsia, preterm labor, fetal growth restriction, oligohydramnios, fetal distress, and congenital diaphragmatic hernia. For most indications, the rationale for administering prenatal sildenafil is based on limited, equivocal data from in vitro studies and rodent disease models. Clinical studies report mild maternal side effects and suggest good fetal tolerance and safety depending on the underlying pathology.

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