Pregnancy Growth Retardation Research Articles

Venous drainage of the human uterus: Respiratory gas studiesin normal and fetal growth-retarded pregnancies

To determine respiratory gas relationships between the uterine veins and umbilical vein in normal and pregnancies complicated by intrauterine growth retardation. Respiratory gases were measured in both uterine veins and the umbilical vein in eight normal and 13 pregnancies with intrauterine growth retardation. No significant differences were found in the placental versus nonplacental uterine veins. There was a significant correlation for umbilical and uterine venous values of PO2 (p less than 0.002) and PCO2 (p less than 0.004) in appropriate-for-gestational-age pregnancies, umbilical venous PO2 was always less than uterine venous PO2, and PCO2 always greater than uterine. The transplacental gradient was significantly higher in intrauterine growth retarded than appropriate-for-gestational-age pregnancies for both POC2 and PCO2. There was a lower uterine oxygen extraction in intrauterine growth retarded pregnancies (p less than 0.05). There is no consistent relationship between placental venous drainage in each uterine vein and placental location. The human placenta simulates a relatively inefficient venous equilibrator and the larger transplacental gradients in intrauterine growth retarded pregnancies may reflect differences in both perfusion pattern and placental structure.

Characterization of placental vascular receptors for atrial natriuretic peptide from normal, pre-eclamptic and growth-retarded pregnancies

Characterization of placental vascular receptors for atrial natriuretic peptide from normal, pre-eclamptic and growth-retarded pregnancies

Placental zinc in normal and intra-uterine growth-retarded pregnancies

The zinc concentration of placental tissue and cord blood in sixteen mothers who gave birth to normal babies was measured. The blood volume of each placenta was estimated from measurements of haemoglobin concentration of placental homogenate and cord blood, and, by deduction, the Zn content of blood-free placental tissue was calculated. Results were compared with eleven mothers whose fetuses showed a low biparietal diameter velocity between 17 and 28 weeks gestation and with ten mothers who gave birth to intra-uterine growth-retarded (IUGR) babies. As expected, placental weight was significantly correlated with infant birth weight. Blood-free placental tissue contained about four times more Zn (approximately 10 micrograms Zn/g) than cord blood (approximately 2.5 micrograms Zn/ml). Concentrations of Zn in blood-free placental tissue were similar in all three groups, but the cord blood Zn of mothers producing IUGR babies was significantly lower than that of the other two groups. Results of the present study suggested that fetal growth retardation in the mothers studied could not be explained by differences in blood-free placental Zn concentration, but that there may be some association between lower cord blood Zn levels and intra-uterine growth retardation.

Cerebral Doppler ultrasound of the human fetus.

Maximal flow velocity waveforms were recorded in the internal carotid artery (ICA), middle cerebral artery (MCA), posterior cerebral artery (PCA) and anterior cerebral artery (ACA) in 55 normal pregnancies and 14 complicated by intrauterine growth retardation between 25 and 41 weeks gestation. In normal pregnancy, acceptable flow velocity waveforms were obtained in the ICA in 89%, in the MCA in 91%, in the PCA in 58% and in the ACA in 64%. A decrease in pulsatility was observed in all four intracranial arteries during the latter weeks of gestation. In growth-retarded pregnancies, pulsatility in all vessels was significantly reduced compared with normal pregnancy, suggesting participation of all major intracranial arteries in a brain-sparing effect in the presence of chronic fetal hypoxia.

Uterine artery flow velocity waveforms in normal and growth-retarded pregnancies

Uterine artery flow velocity waveforms were measured by continuous-wave Doppler ultrasound in 15 normal pregnant women studied from midgestation until term. Results were analyzed by calculation of the pulsatility index and the systolic/diastolic blood pressure ratio. Both indices decreased from 16 to 20 weeks (indicating a lowering of resistance) and thereafter remained stable until term. Resistance was lower when waveforms were recorded directly over the placenta or from the uterine artery close to the placenta. A group of women with severe intrauterine growth retardation were also studied. In preeclampsia, uterine artery resistance was increased in almost all patients. In pregnancies complicated by intrauterine growth retardation of non preeclamptic origin, a wide range of results was obtained.

Birth weight and plasma urate in a heterogeneous population

SummaryPlasma urate levels in 441 singleton pregnancies were analysed to investigate previous observations of raised levels in pregnancies affected by intra-uterine growth retardation. Urate levels were significantly higher after 30 weeks with growth retardation in pregnancies affected by pre-eclampsia. This difference was not demonstrated in normotensive patients. nor among groups in which low birth weight was expected because of racial origin or smoking habit. Among non-smokers. levels were significantly lower before 20 weeks in Asian patients and higher between 31 and 35 weeks in negroes when compared to Caucasians.

Biologic activity and quantification of messenger RNA coding for human chorionic somatomammotropin in normal and intrauterine growth-retarded pregnancies

Total ribonucleic acid (RNA) from human placentas obtained from normal and intrauterine growth-retarded (IUGR) pregnancies was translated in a reticulocyte cell-free system. Synthesis of human chorionic somatomammotropin (hCS) was estimated as a ratio of specific immunoprecipitated protein over total newly synthesized proteins. There is no significant difference between in vitro hCS synthesis directed by placental RNA from normal and IUGR pregnancies. Measurements of messenger RNA sequences coding for hCS, with a hCS complementary DNA probe, indicated that the hCS messenger RNA (mRNA) concentrations were similar for both groups. Low plasma hCS levels in pregnancies associated with growth-retarded fetuses can be explained by their significantly lower placental weights which correlate with their total RNA content. The total capacity of in vitro hCS production per placenta is significantly lower in this type of abnormal pregnancy. There is a good parallelism between the amount of hCS mRNA, its biologic activity tested in a cell-free system, and the secretion of hCS in the maternal circulation. These data suggest that there is no basic intracellular disturbance in hCS synthesis in placentas from fetal growth-retarded pregnancies.

Fetal Adrenal Gland Maturation in Growth-Retarded Twin Pregnancies

Twenty-two twin pregnancies each with one growth-retarded and one normal twin fetus were examined to determine the effects of fetal growth retardation on the maturation of the adrenal gland with respect to cortisol and dehydroepiandrosterone sulphate (DHEAS). The growth-retarded twin fetuses (IUGR) had lower umbilical arterial concentrations of DHEAS than their siblings (IUGR 5.25 +/- 2.4; non-IUGR 6.51 +/- 2.9 mumols/l; p less than 0.01), whereas cortisol concentrations were not statistically different (no labor, IUGR 1,134 +/- 751, non-IUGR 1,140 +/- 958 mumols/l; labor IUGR 2,062 +/- 929, non-IUGR 1,609 +/- 469 mumols/l). These data suggest that while the definitive zone of the fetal adrenal is as well-developed as in non-growth-retarded twins, the fetal zone shows reduced secretory capacity of delta 5-steroids. This supports the hypothesis that in growth retardation the adrenal gland shows features of increased maturation.

Fetal growth retardation and the maternal arterial supply of the human placenta in the absence of sustained hypertension.

In five patients with fetal growth retardation in pregnancies with no or only a moderate and transient rise in blood pressure, vascular lesions in the placental bed spiral arteries were found. These lesions are characterized by less well developed physiological morphological changes, by extensive intimal thickening, by fibrinoid degeneration of the media and by acute atherosis. the recurrent fetal growth retardation in these pregnancies may be the first clinical manifestation of underlying reno-vascular disease.

A Study of Smoking and Pregnancy with Special Reference to Fetal Growth

Abstract. A prospective study of the influence of smoking on pregnancy and its outcome was made of 5272 women in an urban community during 1974/75. Approximately 90 % of the pregnant women in the population took part in the programme. Ultrasonic measurements of the fetal biparietal diameter (BPD) were made from the 18‐20th week (early in the study the first BPD measurements were obtained at 28 weeks). Growth curves of BPD were constructed for each week, separately for the smoking groups (49 %) and the non‐smoking group (51 %) by compiling 5714 BPD measurements, only women subsequently delivered between 266 and 294 days after the last menstrual period were included to avoid erroneously skewed growth profiles. The BPD increased faster during gestation in the non‐smoking group, the difference from the smoking group being significantly apparent from the 28th week onwards and positively correlated to the average number of cigarettes smoked. There was a preponderance within the non‐smoking group for marriage, and preeclampsia; and within the smoking group for abruptio placentae, pre‐term delivery, low birth‐weight, short birth‐length, small head circumference, and small‐for‐gestational‐age. The low birth‐weights were independent of maternal prepregnant weight and weight gain. Compared with data obtained in a similar study in the same community, 1963/64, the prevalence of smoking among pregnant women had increased from 44 % to 49 %. The present study demonstrates the early onset of intrauterine growth retardation in pregnancies of smoking mothers. The results suggest that the fetal growth retardation is a direct pharmacological effect on the fetus rather than an influence resulting from nutritional deprivation and points to appearent inefficiency of the programme deterring women from smoking.