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Objective: Magnetic resonance imaging allows the noninvasive observation of PO2 changes between air breathing and oxygen breathing through quantification of the magnetic longitudinal relaxation time T1. Changes in PO2 are proportional to changes in the longitudinal relaxation rate ΔR1 (where ΔR1=1/T1oxygen-1/T1air). Knowledge of this response could inform clinical interventions using maternal oxygen administration antenatally to treat fetal growth restriction. We present in vivo measurements of the response of the fetal-placental unit to maternal hyperoxia.Design: Prospective cohort.Setting: Large tertiary maternity hospital.Sample: Nine women undergoing low-risk pregnancy (21-33 weeks of gestation) and five nonpregnant adults.Methods: During imaging the air supply to mothers was changed from medical air (21% oxygen) to medical oxygen (100% oxygen) and T1 was monitored over time in both the placenta and fetal brain using a periodically repeated magnetic resonance imaging sequence. To demonstrate that the method could detect a brain response, brain responses from five normal adult volunteers were measured using a similar imaging protocol.Main Outcome Measure: Changes in T1 following oxygen challenge.Results: No significant ΔR1 (P=0.42, paired t-test) was observed in fetal brains. A significant placental ΔR1 (P=0.0002, paired t-test) of 0.02±0.01/s (mean±SD) was simultaneously observed in the same participants. In the brains of the nonpregnant adults, a significant ΔR1 (P=0.01, paired t-test) of 0.005±0.002/s was observed.Conclusion: Short-term maternal oxygen administration does not improve fetal brain oxygenation, in contrast to the response observed in the adult brain. [ABSTRACT FROM AUTHOR]

Objective Magnetic resonance imaging allows the noninvasive observation of Po2 changes between air breathing and oxygen breathing through quantification of the magnetic longitudinal relaxation time T1. Changes in Po2 are proportional to changes in the longitudinal relaxation rate Δ R1 (where Δ R1 = 1/ T1oxygen − 1/ T1air). Knowledge of this response could inform clinical interventions using maternal oxygen administration antenatally to treat fetal growth restriction. We present in vivo measurements of the response of the fetal-placental unit to maternal hyperoxia. Design Prospective cohort. Setting Large tertiary maternity hospital. Sample Nine women undergoing low-risk pregnancy (21-33 weeks of gestation) and five nonpregnant adults. Methods During imaging the air supply to mothers was changed from medical air (21% oxygen) to medical oxygen (100% oxygen) and T1 was monitored over time in both the placenta and fetal brain using a periodically repeated magnetic resonance imaging sequence. To demonstrate that the method could detect a brain response, brain responses from five normal adult volunteers were measured using a similar imaging protocol. Main outcome measure Changes in T1 following oxygen challenge. Results No significant Δ R1 ( P = 0.42, paired t-test) was observed in fetal brains. A significant placental Δ R1 ( P = 0.0002, paired t-test) of 0.02 ± 0.01/s (mean ± SD) was simultaneously observed in the same participants. In the brains of the nonpregnant adults, a significant Δ R1 ( P = 0.01, paired t-test) of 0.005 ± 0.002/s was observed. Conclusion Short-term maternal oxygen administration does not improve fetal brain oxygenation, in contrast to the response observed in the adult brain. [ABSTRACT FROM AUTHOR]

Problem: Inflammation during pregnancy has devastating consequences for the placenta and fetus. These events are incompletely understood, thereby hampering screening and treatment., Method of Study: The inflammatory profile of villous tissue was studied in pregnancies at high-risk of placental dysfunction and compared to uncomplicated pregnancies. The systemic inflammatory profile was assessed in matched maternal serum samples in cases of reduced fetal movements (RFM)., Results: Placentas from RFM pregnancies had a unique inflammatory profile characterized by increased interleukin (IL)-1 receptor antagonist and decreased IL-10 expression, concomitant with increased numbers of placental macrophages. This aberrant cytokine profile was evident in maternal serum in RFM, as were increased levels of alarmins (uric acid, HMGB1, cell-free fetal DNA)., Conclusion: This distinct inflammatory profile at the maternal-fetal interface, mirrored in maternal serum, could represent biomarkers of placental inflammation and could offer novel therapeutic options to protect the placenta and fetus from an adverse maternal environment., (© 2014 The Authors. American Journal of Reproductive Immunology Published by John Wiley & Sons Ltd.)

The regulation of placental anion transport influences fetal accretion and placental homeostasis. We investigated whether efflux of 125I- or 36Cl- from multinucleated cytotrophoblast cells derived from human term placenta is regulated by one of three stimuli: (a) the calcium ionophore A23187, (b) a 'cocktail' of agents designed to raise intracellular levels of cAMP, (c) a hyposmotic solution. After loading with the appropriate isotope for 2 h and thorough washing, cells were exposed to sequential aliquots of buffer applied and removed each minute. Following an equilibration period of 5 min one of the stimuli was applied at room temperature At the end of the experiment the cells were lysed to give a lysate count which was used to express the count obtained from each aliquot as percentage efflux of that possible for that minute. The cAMP 'cocktail' and A23187 were applied for 5 min; the hyposmotic solution was applied for 10 min. The results for 125I- at 7 min showed that the mean efflux in the presence of hyposmotic shock was greater than control (5.7 +/- 1.0% min-1 versus 2.2 +/- 0.1% min-1, respectively; mean +/- S.E.M., n = 4 placentas). Similarly mean efflux at 6 min in the presence of A23187 was also significantly greater than control (6.5 +/- 1.9% min-1 versus 2.6 +/- 1.0% min-1, respectively, n = 3 placentas). The mean efflux in the presence of the cAMP cocktail was not different from control at any time point. The results were qualitatively the same if 36Cl- was used in the place of 125I- and when the experiment was performed with 36Cl- in a HCO3- buffer gassed with CO2. Mean 125I- efflux at 6 min in response to hyposmotic challenge was 33% less (P < 0.01) in the presence of 1 mM 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) and 37% less (P < 0.005) in the presence of 10 microM tamoxifen but no different if the hyposmotic solution was nominally calcium free. We conclude that there are differential effects of second messengers on anion efflux from the differentiated cytotrophoblast cells.

Feto-maternal vascular (PD(F-M)) and amniotic maternal (PD(A-M)) potential differences were measured simultaneously on seven occasions in six conscious pigs of 100-106 days gestation. Resting values of PD(F-M) and PD(A-M) were not significantly different although the range was wide. Fetal intravascular injection of 20 microg adrenaline, but not of saline, was associated with a prompt reversible change, of equal magnitude, in both PD(F-M) and PD(A-M). In some experiments polarity was reversed. Feto-amniotic potential difference did not change. There was no change in fetal plasma K+ and Na+ concentrations. Because of the simultaneous and equal alterations in PD(F-M) and PD(A-M) following adrenaline and the anatomical configuration of the pig conceptus, we conclude that the catecholamine modifiable component of PD(F-M) is generated by electrogenesis in the pig placenta, probably by its chorionic (trophoblastic) cell layer.

A disturbed calcium homeostasis characterizes diabetic pregnancy. This study documents changes in bone mineral composition in diabetic pregnant rats and examines the effect of insulin replacement. Control pregnant (CP), diabetic pregnant (DP) and insulin-treated DP (DPi) rats were assessed for femoral calcium and magnesium content, bone mineral density (BMD) and the ratio of hypertrophic to maturing and proliferative cells in the femoral growth plate. DP rats showed a significantly (P < 0.01) lower body weight, femoral weight and length than CP rats. Femoral calcium and magnesium content was also significantly (P < 0.05) lower in DP rats, as was ash weight. When calcium and magnesium were normalized for ash weight no significant differences were apparent. A significantly (P < 0.05) lower total BMD at the distal femur was seen in DP rats. This comprised a significantly (P < 0.01) lower trabecular BMD with no significant change in cortical BMD. A significantly (P < 0.05) higher ratio of hypertrophic to maturing and proliferative cells of the femoral growth plate was evident in DP animals. DPi rats showed normal blood glucose concentrations and femoral growth plate histology. DPi rats also showed normal femoral weight and length but only partially restored femoral ash weight and mineral content. Insulin failed to normalize total or trabecular BMD. Diabetes mellitus clearly has a marked effect on bone growth and mineral content in pregnancy which may be relevant to overall calcium homeostasis. The lower bone growth, bone calcium content and trabecular BMD may be unfortunate consequences of the marked hypercalciuria reported elsewhere in diabetes and may serve to maintain normocalcaemia in the disease.