Long term consequences of fetal deprivation.
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Biomedical subjects
Publications and source records attributed to F E Hytten.
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A number of compounds in pregnancy blood reach a maximum or minimum concentration at around 20-24 weeks of pregnancy, a period of conspicuous clinical tranquility. The compounds mostly derive from either fetal tissue or decidua and it is suggested that they may be part of an elaborate mechanism which controls invasion of the uterine wall by trophoblast.
The effect of maternal acidosis on fetal acid-base balance was studied in a dual circuit perfusion of a single cotyledon in normal, term, human placentas. Both the fetal and maternal (intervillous) circulations were perfused with a Krebs-Ringer solution adjusted to pH values between 7.35 and 7.45. After a control period, the perfusate in the maternal circulation was replaced by an acidified medium (mean pH 7.06) for 30 min. This was followed by a second control period of 30 min during which the acidified maternal perfusate was replaced with the original medium. During the 30 min of maternal acidosis, fetal vein pH was not significantly altered despite the large decrease in maternal artery pH, but there was an efflux of total CO2 (tCO2) from the placenta into the maternal circulation which was not matched by an influx of tCO2 from the fetal circulation. The tCO2 transferred was in the form of bicarbonate rather than dissolved CO2, but the maximal rate of tCO2 transfer of in the form of bicarbonate was lower than the rate of placental transfer of tCO2 necessary in vivo. It is probable therefore that bicarbonate does not play a major role in placental CO2 transfer but the placental tissue bicarbonate pool may play an important part in buffering the fetus against changes in maternal pH or blood gas status.
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Scalp blood flow and transcutaneous (tc) PO2 were measured in four fetal lambs at 130-135 days of gestation. Scalp blood flow was measured by the xenon clearance technique using a technetium source to correct for changes in distance from the detector. The effect of circular pressure, the so-called "tonsure effect" on scalp flow and tcPO2, was evaluated by pressing a ring on the scalp. A circular pressure between 20-30 mmHg markedly reduced local scalp blood flow and was sufficient to reduce tcPO2 to zero. We found evidence of significant recirculation of xenon in the fetal circulation indicating right-left shunting. This study showed that the tonsure effect seriously affected scalp blood flow and tcPO2 in the fetus.
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Amniotic fluid samples were obtained at induction of labour in 64 women; in 15 of these there was meconium staining of the amniotic fluid; the remainder showed no signs of fetal distress. Using high pressure liquid chromatography, compared to the samples from normal patients there were highly significantly raised levels of hypoxanthine, xanthine and uridine in the meconium stained samples; oxypurines in the meconium itself could not explain the difference. Where serial samples were obtained during labour by intrauterine catheter, a terminal rise in oxypurine levels was apparent. Where the proportion of oxypurine present as hypoxanthine exceeded one per cent in amniotic fluid at the time of induction, there was a significantly greater occurrence of late fetal heart rate decelerations in the ensuing labour. These findings are consistent with other evidence that when tissues become hypoxic the metabolic products of nucleotide breakdown escape from the cells and appear in extracellular fluid. Oxygen lack in the fetus probably causes loss of these compounds from the hypoxic kidneys to the urine so that they appear in amniotic fluid.
Hypoxanthine, xanthine, inosine, urate and uridine, were measured in 149 samples of umbilical cord plasma using high pressure liquid chromatography. In spite of a good correlation with the simpler oxygen consumption method for measuring hypoxanthine, there was no clear discrimination between hypoxic and well oxygenated infants, although mean concentrations were higher in infants with well defined criteria of intrapartum hypoxia or bith asphyxia, there was overlap with the normal range. Fetal scalp blood samples were also found to be clinically unhelpful in the diagnosis of intrapartum hypoxia, at least in part due to variable degrees of haemolysis in the specimens. There were poor correlations between hypoxanthine concentrations and those of hydrogen ion, base deficit and lactate. Uridine concentrations were significantly higher in arterial cord blood than in venous cord blood but hypoxanthine or xanthine concentrations did not show this difference.
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Capillary blood-flow and tissue oxygenation of the scalp and/or forearm skin were measured in the three adult volunteers. Skin pressure required to occlude circulation was much lower for the scalp than for the forearm skin, and tissue oxygenation fell rapidly when capillary blood-flow fell below about 3 ml/100 g tissue/min. Since scalp circulation is not representative of the general circulation when pressure is applied, the tissue oxygenation level of the fetal scalp in labour (obtained by direct sampling or by transcutaneous electrodes) is not a good indicator of the well-being of a fetus.
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