Observations on the Oxygenation of the Foetus in Normal and Abnormal Pregnancy

Mackay, Rachel B.

doi:10.1111/j.1471-0528.1957.tb02619.x

Cited by 77 publications

(13 citation statements)

References 17 publications

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“…These results have been confirmed by MacKay (1957), whereas no such change has been observed by MacKinney et al (1955), BancroftLivingston and Neill (1957) or Rooth and Sjbstedt (1957). Recently Tumbull and Baird (1957) and Walker and Turnbull (1959) have stated that this decrease only occurs in primigravidae.…”

Section: Archives Of Disease In Childhoodsupporting

confidence: 75%

The Oxygen Tension of the Blood in the Umbilical Cord and the Intervillous Space

Sjöstedt

Rooth

Caligara

1961

Obstetrical & Gynecological Survey

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Section: Archives Of Disease In Childhoodsupporting

confidence: 75%

The Oxygen Tension of the Blood in the Umbilical Cord and the Intervillous Space

Sjöstedt

Rooth

Caligara

1961

Obstetrical & Gynecological Survey

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“…A marked reduction in uterine and placental blood flow in toxemic patients has been demonstrated by several workers (22)(23)(24). These observations probably explain the low oxygen content of umbilical cord blood of infants at delivery of toxemic mothers (25)(26)(27) The lactic acid level fell in three of four patients and the clearance ratio rose in all four patients, following delivery. exchange and its quantitative characteristics are thus unresolved, but it would be reasonable to assume that the more hypoxic fetus of a pre-eclamptic patient, depending more upon anaerobic metabolism, produces greater than normal quantities of lactic acid which might then influence maternalfetal exchange so that the rate of net lactate transfer into maternal blood is increased.…”

Section: Resultsmentioning

confidence: 99%

The Role of Lactic Acid in the Reduced Excretion of Uric Acid in Toxemia of Pregnancy *

Handler¹

1960

J. Clin. Invest.

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Wlhen Chesley and Williams demonstrated low uric acid excretion in toxemiiic patients,1 they noted that the reduction in renal urate clearance was relatively greater than the reduction in glomerular filtration rate (1). This relationship has been confirmed (2) and is striking when c-ompared with observations on urate excretion in normal slibjects and patients with renal disease. It is generally accepted that tunder normal circtumstances serum urate is completely filtered at the glomertulus and that 5 to 10 per cent of filtered turate appears in the urine (3) ; net tubular reabsorption accounts for the other 90 to 95 per cent. Coombs and co-workers (4), in a sttudy of subjects with various degrees of renal imiipairment, found that as glomerular filtration rate fell, a progressively larger portion of filtered urate was excreted in the urine, uric acid clearance increasing to over 20 per cent of glomerular filtration rate. In preeclamptic and eclamptic patients, althotugh glomerular filtration rate is reduced, the ratio of urate clearance to glomerular filtration rate is often lower than normal. Unless there is a redtuction in the filtrability of serum turate, explanation of the low ratio of uric acid clearance to glomiiertular filtra-*

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“…MacKay (37) noted a marked umbilical arterial hypoxemia in a small number of IDM's at delivery in the only study available in which 02 content was measured in umbilical vessels. Naeye (38) …”

Section: Discussionmentioning

confidence: 99%

Effects of chronic fetal hyperglycemia upon oxygen consumption in the ovine uterus and conceptus.

Philipps¹,

Porte²,

Stabinsky³

et al. 1984

J. Clin. Invest.

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Abstra ct. Hyperglycemia has been shown to induce arterial hypoxemia in the chronically catheterized fetal sheep. To investigate the mechanism behind this glucose-induced hypoxemia, eight pregnant ewes and their fetuses were studied. Fetal glucose infusion (1 1.9±0.6 mg glucose/kg per min) was associated with a doubling of the fetal plasma glucose concentration with concomitant elevation of the umbilical vein-distal arterial 02 content difference by 24 h of infusion (P < 0.01). Calculated fetal 02 consumption increased from 8.1±0.4 ml/kg per min in the control period to a maximum value of 10.6±0.3 ml/kg per min by third infusion day (P < 0.01), which is an increase of -30%. The degree of stimulation of fetal 02 consumption was related to the degree of fetal hyperglycemia but not to the degree of fetal hyperinsulinemia. The increase in fetal 02 consumption was accompanied by a significant increase in fetal 02 extraction with no change in either fetal 02 delivery or fetal blood 02 affinity. In addition, fetal hypercapnea with a mild fetal respiratory acidosis was induced by fetal hyperglycemia. The increase in fetal arterial Pco2 was linearly related (P < 0.001) to the magnitude of increase in fetal 02 consumption. These studies suggest that chronic fetal hyperglycemia induces a state ofaccelerated fetal oxidative metabolism and may be important in explaining the etiology behind certain unusual findings in human infants of diabetic mothers.

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Observations on the Oxygenation of the Foetus in Normal and Abnormal Pregnancy

Cited by 77 publications

References 17 publications

The Oxygen Tension of the Blood in the Umbilical Cord and the Intervillous Space

The Oxygen Tension of the Blood in the Umbilical Cord and the Intervillous Space

The Role of Lactic Acid in the Reduced Excretion of Uric Acid in Toxemia of Pregnancy *

Effects of chronic fetal hyperglycemia upon oxygen consumption in the ovine uterus and conceptus.

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