Intrauterine Growth Retardation Pregnancies Research Articles

Reviewing placental volumetry and thickness and its correlation with adverse feto maternal outcome - A cross sectional study in Western India

BACKGROUND: Placenta performs several functions including respiration, nutrition, and excretion for the fetus when playing a central role in regulating metabolic, endocrinological, and immunological functions during pregnancy. OBJECTIVE: To analyze the putative correlation of placental parameters including volume and thickness with adverse maternofetal outcomes. METHODOLOGY: A longitudinal observational study was undertaken for 2 years. The sample size was calculated, which was 140. Data were collected, and fetomaternal outcomes of gestational diabetes mellitus (GDM), gestational hypertension (HTN), preeclampsia, and intrauterine growth retardation (IUGR) were derived. A correlation was studied between placental volume (PV) and placental thickness (PT) with fetomaternal outcomes. RESULTS: Approximately half (42.85%) of the study population were primigravida, with overall mean age being 22.67 ± 2.94 years. 46 subjects had adverse fetomaternal outcomes in the form of gestational HTN, preeclampsia, GDM, and IUGR. The most frequent adverse outcome noted was IUGR in 19 cases (41.29%). Among the study population, 90% were term deliveries and 10% were preterm. Spontaneous vertex delivery was seen in 74.29% of the cases. 24.29% of the cases underwent lower segment cesarean section and 1.43% underwent vacuum-assisted delivery. The PV and PT (mm) were compared in healthy subjects with HTN, GDM, and IUGR pregnancies in all three trimesters. A strong correlation (R = 0.96, 95% confidence interval = 0.95–0.98) between birth weight with placental weight was noted. The difference between the means of PV during the first, second, and third trimester and hypertensive disorders in pregnancy was not statistically significant; among GDM and non-GDM patients, was statistically significant in the first and second trimester; and among IUGR and non-IUGR patients, was seen during the third trimester. Similarly, the difference between the means of PT in all trimesters and hypertensive disorders in pregnancy was not statistically significant; among GDM and non-GDM patients, a statistically significant association was seen during the second trimester; and among IUGR and non-IUGR patients, a statistically significant association was seen during the third trimester. CONCLUSIONS: PV in the 1st, 2nd, and 3rd trimesters is significantly less in patients with HTN and IUGR. PV is a predictor of adverse fetomaternal outcomes. Hypertensive subjects had thin placenta with low PV. Hypertensive subjects had thin placenta with low PV. IUGR subjects had thin placenta with low PV. Diabetic subjects had thick placenta. PT is also a predictor of adverse fetomaternal outcomes. Placental weight is known to correlate with fetal weight at term.

Utility of sonographic transcerebellar diameter in the assessment of gestational age in normal and intrauterine growth-retarded fetuses.

The fetal cerebellum has been shown to be least affected by external pressures and molding during pregnancy and therefore might provide more accurate estimation of GA. To study the utility of transcerebellar diameter (TCD) measured by ultrasound for the detection of GA in normal and intrauterine growth-retarded (IUGR) fetuses. This cross-sectional study comprised 500 antenatal patients with a GA between 14 and 39 weeks and who were certain of their last menstrual periods. The TCD was measured ultrasonographically and the corresponding GA was determined. The GA was also determined with other customarily used sonographic parameters such as biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), and femur length (FL) and compared with TCD. Data of normal pregnancy patients was used to formulate nomograms by taking the 5th, 50th, and 95th percentile measurements. TCD to AC ratio was also calculated in both normal (n = 424) and IUGR pregnancies (n = 76). TCD showed significant correlation with gestational age (GA) measured by last menstrual period (LMP) as well as with GA calculated with other biometric fetal parameters. TCD also showed significant correlation with GA in normal (R2 = 0.979) as well as with IUGR pregnancies (R2 = 0.942). TCD to AC ratio remained fairly constant in normal pregnancies while it was increased in IUGR pregnancies. TCD and TCD/AC ratio can be employed as an objective parameter to establish the GA in normal as well as IUGR pregnancy cases.

Comparison of placental elasticity in normal and intrauterine growth retardation pregnancies by ex vivo strain elastography.

To compare the placental elasticity in fetuses with or without intrauterine growth restriction (IUGR). One hundred pregnant women (50 IUGR and 50 healthy) with anteriorly located placenta were evaluated during the third trimester of pregnancy. Measurements were carried out by a machine that has a real-time elastographic ultrasonography feature. After obtaining the optimum image, three areas (subcutaneous tissue, center, and the edge of the placenta) were provided to identify the placental strain values. Then, the placental strain ratio (PSR) value was calculated automatically. Two groups compared in terms of their PSR values. There was a significant difference in placental elasticity between the groups (P < 0.001). PSR value was 2.8 ± 1.2 in the IUGR group and 1.3 ± 0.6 in the control group. A PSR value of 1.78 had an 86% sensitivity (OR 4.3) and 80% specificity (OR 0.17) in IUGR cases. The positive predictive value was 81.1% and the negative predictive value was 85.1% for this cut-off value. We have shown that placental strain ratio is increased during the third trimester of pregnancy in fetuses with IUGR. Increased stiffness and elasticity may be responsible for the onset of IUGR in some cases.

Estimation of Placental Thickness by Ultrasonography and its Correlation with Gestational Age in Normal and Intrauterine Growth Retardation Pregnancies in Late 2nd And 3rd Trimester

Estimation of Placental Thickness by Ultrasonography and its Correlation with Gestational Age in Normal and Intrauterine Growth Retardation Pregnancies in Late 2nd And 3rd Trimester

Systemic Lupus Erythematosus and Pregnancy Outcome in Tertiary Level Hospital of Nepal

Introduction: Systemic Lupus Erythematosus is an autoimmune disease frequently prevalent in women starting from early childhood and towards the reproductive age. Pregnancy with SLE has always imposed great risk both to the mother and the fetus. A multidisciplinary approach with Nephrologist, neonatologist and senior obstetrician during remission leads to a favorable response, through limitation and complications with the use of drugs impose difficulties in their management.Materials and Methods: A prospective, descriptive study was conducted in the Department of Obstetrics and Gynecology and Nephrology at Tribhuvan University Teaching Hospital, for 2 years, from June 2015 to 2017. The study included obstetrical and related complications with outcome in pregnant patients with Systemic Lupus Erythematosus.Results: A total of 19 cases were analyzed of which 15 (79%) had a viable pregnancy and 4 (21%) abortions. Of thirteen cases, 4 (21%) had antiphospholipid antibody syndrome, 8 (42.1%) lupus, and membranous glomerulonephritis and 1 (5.2%) lupus optic neuropathy with loss of vision. All the patients were under drug therapy, like prednisolone, azathioprine, hydroxychloroquine, aspirin, low molecular weight Heparin, tacrolimus, and cyclophosphamide. Only 2 (10.5%) of 19 developed severe pre-eclampsia. There were 12 (80%) term and 3 (20%) each of preterm and intrauterine growth retardation pregnancies with 1 (6.6%) neonatal death (NND) and 1 (5.2%) maternal mortality.Conclusions: Multidisciplinary approach and planned pregnancy reduces the risk of probable complications in the patient resulting to a decreased morbidity and mortality.

Histopathological study of placentae in intrauterine growth retardation pregnancies in a tertiary care hospital and correlation with fetal birth weight

Background: Intra uterine Growth Retardation is the most significant factor of perinatal mortality. The aim of this study was to assess the histopathological changes in the placenta in association with IUGR and correlation with fetal birth weight.Materials and Methods: A total of 100 placentae were included. Twenty five normal placentae and 75 placentae were from IUGR pregnancies were included.Results: Intervillous fibrin deposition (64%), increased syncytial knotting (64%), stromal fibrosis (65%), cytotrophoblastic hyperplasia (44%) and basement membrane thickening (40%) were seen along with hypovascular villi and infraction were present in 32% and 28% respectively. These changes were seen less in the control group (p&lt;0.001). Statistically significant association between the birth weight and microscopic changes (chi square=19.543, degree of freedom=4, p&lt;0.005) was observed.Conclusion: Severity of IUGR is related to the microscopic change in the placenta. The number and severity of microscopic changes in IUGR placentas increased with decreasing fetal birth weight.

Placental Thickness: Its Correlation with Ultrasonographic Gestational Age in Normal and Intrauterine Growth-Retarded Pregnancies in the Late Second and Third Trimester

The aim was to study the correlation of placental thickness, measured at the level of the umbilical cord insertion, with the ultrasonographic gestational age in normal and IUGR pregnancies in the late second and third trimester. A total of 498 patients were observed for correlation of the placental thickness with ultrasonographic gestational age and their outcomes by dividing them into Group A (outcome fetal weight<2,500g, n=122) and Group B (fetal weight>2,500g, n=376). The mean placental thickness was calculated at the umbilical cord insertion in both groups along with ultrasonographic fetal age and estimated fetal weight. The mean values of placental thickness along with respective standard deviation were calculated from the 24th to 39th week of gestational age. A positive correlation was observed between placental thickness and ultrasonographic gestational age in both groups (p value of 0.01), with Pearson's correlation coefficient ("r") values of 0.325 in Group A and 0.135 in Group B. Regression analysis yielded linear equations of relationship with placental thickness and gestational age in both groups. The placental thickness was also found to be lower in Group A between 26 and 27weeks and 30 and 31weeks, having mean values of 2.48±0.063cm (p value of 0.042) and 2.76±0.552 (p value of 0.05) in Group A as compared to 3.04±0.25 and 3.13±0.183cm in Group B. Placental thickness measured at the level of umbilical cord insertion can be used as an accurate sonographic indicator in assessment of gestational age in singleton pregnancies because of its linear correlation.

English

Abstract Introduction Placenta is the maternal–foetal contact zone. The placentas of ‘idiopathic’ intrauterine growth retardation babies may hold the key to the aetiology of growth restriction. It was noted by most workers that in cases of intrauterine growth retardation placentas, there were some abnormal positions of insertion of umbilical cords, placental weight and volume was significantly lower than the controls and they also had smaller diameters. The greater placental coefficient in intrauterine growth retardation indicates that though both placentas and babies in intrauterine growth retardation had less weight, placental sizes were not relatively less. This article aims to review literature to identify any morphological and structural peculiarities of placenta that might contribute to development of idiopathic intrauterine growth retardation. Discussion Light microscopy suggested that syncytiotrophoblastic lining was more degenerated and a number of syncytial knots increased in intrauterine growth retardation placentas than that of the control placentas. X cells were present in both the cases, though more in intrauterine growth retardation. Intravillous and perivillous fibrin depositions were markedly increased in intrauterine growth retardation; also there were more hypovascular/avascular villi and large areas of infarction. Conclusion Review of the literature to establish any relationship between placental histomorphometric changes and intrauterine growth retardation suggests that intrauterine growth retardation pregnancies are associated with reductions in villous tree elaboration, particularly affecting the volume and surface area of terminal and intermediate villi, thereby restricting surface area over which foetomaternal exchange may occur. Thus, placental oxygen transfer might be reduced, thereby restricting foetal growth and development.

Increased Expression and Altered Methylation of HERVWE1 in the Human Placentas of Smaller Fetuses from Monozygotic, Dichorionic, Discordant Twins

BackgroundThe human endogenous retroviral family W, Env(C7), member 1 gene (HERVWE1) is thought to participate in trophoblast cell fusion, and its expression is diminished in the placentas of singleton intrauterine growth-retarded pregnancies. However, there is limited information about the role of HERVWE1 in discordant fetal growth in twins. This study was to compare HERVWE1 gene expression between the placentas of discordant monozygotic twins and to identify its regulation by methylation.Methodology/Principal FindingsFetuses from twenty-one pairs of monozygotic, dichorionic, discordant twins were marked as “smaller” or “larger” according to birth weight. Placental HERVWE1 mRNA and protein expression profiles were analyzed using quantitative RT-PCR and immunohistochemistry (IHC) staining. Methylation profiles of the HERVWE1 promoter region were analyzed using a pyrosequencing assay. DNA methyltransferase (DNMT) transcript levels were analyzed by RT-PCR. 5-methyl cytosine (5-MC) was stained using an immunohistochemical assay. There was a significant negative correlation between HERVWE1 mRNA levels and birth weight in twins (P<0.01). Whereas the mean methylation level of the HERVWE1 promoter region was diminished in the smaller group in discordant twins(P<0.01), increased mRNA and protein levels of HERVWE1 were found in smaller fetuses compared with larger fetuses in discordant twins(P<0.01). There was no significant difference in 5-MC staining intensity between discordant twins (P>0.05). The DNMT3b3 mRNA levels in the smaller group were significantly downregulated compared with the larger group in discordant twins(P<0.05), whereas the DNMT3b7 mRNA levels in the smaller group were significantly upregulated compared with the larger group in discordant twins(P<0.05).Conclusions/SignificanceIn discordant, monozygotic, dichorionic twins, HERVWE1 expression was higher in smaller fetuses and lower in larger fetuses. Methylation of the HERVWE1 gene promoter region may participate in the regulation of HERVWE1 gene expression in discordant twin pregnancies.

Serum nitric oxide syntheses and lipid profile of the mothers with IUGR pregnancies uncomplicated with preeclampsia. Does insulin resistance matter?

Insulin resistance in late pregnancy increases nutrition availability in maternal circulation. Moreover, it is the leading cause of oxidative stress in pregnant women. Herein, we aimed to define the correlation between insulin resistance, serum inducible nitric oxide (iNOS) and serum lipid levels in patients with intrauterine growth retardation (IUGR) pregnancies and controls. We performed a cross sectional study of IUGR pregnancies uncomplicated with preeclampsia as cases and age, body mass index, parity and gestational age matched pregnant women as controls. We quantified serum insulin, fasting blood sugar (FBS), iNOS and lipid profile of the cases and controls. Serum total cholesterol and LDL-C were significantly lower when serum iNOS, FBS, insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels were significantly higher in patients with IUGR pregnancies. There was not any significant difference in serum iNOS levels between patients and controls (12.4 ± 2.1 vs. 11.1 ± 1.9; p = 0.52) after multiple adjustment for HOMA-IR. Serum iNOS levels were significantly correlated with maternal serum insulin, triglyceride and HOMA-IR levels in patients with IUGR pregnancies when there was not such a correlation in controls. We showed a positive correlation between insulin resistance and markers of oxidative stress like iNOS in IUGR pregnancies.

Gender-Related Changes in Magnetocardiographically Determined Fetal Cardiac Time Intervals in Intrauterine Growth Retardation

Prenatal growth deficiencies as well as gender have been associated with cardiovascular disease in later life. It is also known that the duration of fetal cardiac time intervals (CTI) are dependent on fetal development. The aim of this work was to examine the relationship between fetal CTI in healthy and intrauterine growth retardation (IUGR) fetuses, taking gender into account. A total of 269 magnetocardiograms (MCG) were obtained in 47 healthy and 27 IUGR pregnancies. In each signal-averaged MCG, durations of CTI were determined. Age- and heart rate-corrected values were compared between normal and IUGR fetuses separately with respect to gender. Overall, there was an association between atrial and ventricular conduction times and estimated fetal body weight. In female fetuses, IUGR was associated with shorter P WAVE, PQ segment, PR interval, and QRS complex and longer STT and QT intervals. For males, this was so only for P wave, QRS complex, and STT interval. The shortening of conduction times in IUGR may be explained by reduced cardiac muscle mass associated with lower body weight. On the other hand, the gender-specific differences, particularly in the IUGR fetuses may be due to hormonal factors.

124 Maternal Blood S100B Levels in Pregnancies Complicated by Fetal Growth Restriction May Early Predict the Occurrence of Intraventricular Hemorrhage

The aim of these present study was to evaluate maternal levels of S100B (a neural protein found in high concentrations in biological fluids after cell injury in the nervous system), in pregnancies complicated by intrauterine growth retardation (IUGR) and to correlate after their measurements with postnatal intraventricular hemorrhage (IVH) occurrence. A case-control study in pregnant women complicated by IUGR(n= 106) of whom a subgroup (n=26) developed postnatal IVH, and a group of normal pregnancies (n=212) matched for gestational age served as control. Ultrasound scanning, Doppler velocimetry patterns (in the utero-placental and in the middle cerebral artery vessels), and maternal blood samples were collected before birth in all women with IUGR. After birth routine laboratory parameters, cerebral ultrasound patterns and neurological examination were recorded in IUGR and control newborns.Maternal S100B levels were significantly (P<0.001) higher in IUGR pregnancies complicated by postnatal IVH, than in those who did not and in controls. At a cut-off of 0.72 mg/L S100B achieved a sensitivity of 99.3% (C.I.95%: From 86.7 to 100) and a specificity of 98.2% (C.I.95%: From 94.3 to 99.8) as a single marker for prediction of IVH (area under the ROC curve: 0.991). The probability of IVH was 8.17% in the whole study population, 93% (C.I.95%: 83.6–100%) when S100B levels were found above the thresholds defined by the ROC curve analysis, and 0% (C.I.95%: 0–2.5%) if they were found unaltered. Maternal S100B assessment may represent an useful tool for the early suspect of postnatal IVH.

Intrauterine growth retardation is associated with reduced activity and expression of the cationic amino acid transport systems y+/hCAT-1 and y+/hCAT-2B and lower activity of nitric oxide synthase in human umbilical vein endothelial cells.

Intrauterine growth retardation (IUGR) is associated with vascular complications leading to hypoxia and abnormal fetal development. The effect of IUGR on L-arginine transport and nitric oxide (NO) synthesis was investigated in cultures of human umbilical vein endothelial cells (HUVECs). IUGR was associated with membrane depolarization and reduced L-arginine transport (V(max)= 5.8+/-0.2 versus 3.3+/-0.1 pmol/microg protein per minute), with no significant changes in transport affinity (K(m)=159+/-15 versus 137+/-14 micromol/L). L-Arginine transport was trans-stimulated (8- to 9-fold) in cells from normal and IUGR pregnancies. IUGR was associated with reduced production of L-[3H]citrulline from L-[3H] arginine, lower nitrite and intracellular L-arginine, L-citrulline, and cGMP. IUGR decreased hCAT-1 and hCAT-2B mRNA, and increased eNOS mRNA and protein levels. IUGR-associated inhibition of L-arginine transport and NO synthesis, and membrane depolarization were reversed by the NO donor S-nitroso-N-acetyl-L,D-penicillamine. In summary, endothelium from fetuses with IUGR exhibit altered L-arginine transport and NO synthesis (L-arginine/NO pathway), reduced expression and activity of hCAT-1 and hCAT-2B and reduced eNOS activity. Alterations in L-arginine/NO pathway could be critical for the physiological processes involved in the etiology of IUGR in human pregnancies.

Circulating S100beta protein is increased in intrauterine growth-retarded fetuses.

To determine whether S100beta, an acidic calcium-binding protein previously demonstrated as a reliable indicator of a brain lesion, could be helpful in the detection of brain distress in intrauterine growth-retarded (IUGR) fetuses, we studied, by a case-control study, the correlation between S100B protein and the degree of fetoplacental blood flow impairment. Maternal and umbilical blood samples and placental tissue specimens were collected at delivery from IUGR pregnancies with normal (n = 10) or abnormal (n = 10) umbilical artery Doppler findings and from 40 uncomplicated pregnancies. S100beta protein levels were measured by means of a specific RIA, and flow velocimetry waveforms were recorded from uterine, umbilical, and fetal middle cerebral arteries. Overall mean S100beta proteins in umbilical plasma levels were higher (p < 0.05) in IUGR patients (121.8 +/- 70.4 fmol/mL) than in control patients (54.7 +/- 21.9 fmol/mL). IUGR fetuses with redistribution of blood flow showed the higher concentration of the protein (163.7 +/- 55.2 fmol/mL). Fetal S100beta concentrations correlated with middle cerebral artery pulsatility index (r = -0.536, p < 0.03) and with umbilical artery pulsatility index to middle cerebral artery pulsatility index ratio (r = 0.469, p < 0.03). No difference in the localization or intensity of S100beta staining in the placental tissues or cord between uncomplicated and IUGR pregnancies was found. This study provides evidence that circulating S100beta protein is increased in IUGR fetuses and correlates with cerebral hemodynamics, suggesting that it may represent an index of cerebral cell damage in the perinatal period.

Expression of C-Type Natriuretic Peptide in Human Placenta and Myometrium in Normal Pregnancies and Pregnancies Complicated by Intrauterine Growth Retardation

Objective: C-type natriuretic peptide (CNP) is a vasoactive hormone and the endothelial component of the natriuretic peptide system. At present, nothing is known about CNP expression in human reproductive tissue. Since CNP shows antimitogenic and vasodilatative properties, it was the aim of the study to investigate whether CNP expression is altered in placenta and myometrium from pregnancies complicated by intrauterine growth retardation. Methods: CNP expression was examined by RNase protection assay in human placenta and myometrium from six normal term pregnancies, six pregnancies with preterm delivery and six pregnancies complicated by intrauterine growth retardation (IUGR). Results: In placenta and myometrium, CNP expression levels did not differ between term and preterm pregnancies (40 vs. 28 weeks of gestation). In pregnancies with IUGR (34 weeks of gestation) placental CNP expression was significantly decreased (100.00 ± 18.6 vs. 67.09 ± 8.7; p < 0.05). In the myometrium from IUGR pregnancies CNP expression was significantly increased to 191.48 ± 42.5 (vs. 100.00 ± 15.4; p < 0.05). Conclusions: CNP is expressed in human placenta and myometrium with no dependency on gestational age in the third trimester. Pregnancies with IUGR show an opposite regulation of CNP in placenta and myometrium, which indicates an organ-specific function of the peptide in human reproductive tissue.

Expression of insulin-like growth factor-I and placental growth hormone mRNA in placentae: a comparison between normal and intrauterine growth retardation pregnancies.

Intrauterine growth restriction (IUGR) is generally defined as the pathological restriction of fetal growth resulting in a fetus with birth weight below the 10th percentile for gestational age. Almost 75% of IUGR cases develop during third trimester. Studies on animals (rodents and sheep) as well as humans suggest that insulin-like growth factor-I (IGF-I), under the influence of placental growth hormone (PGH) plays crucial roles in fetal growth regulation during this period. Limited data are available with regard to IGF-I and PGH in placentae of normal and IUGR births. Therefore, in the present study, IGF-I and PGH mRNA expression has been studied in term placentae of normal (n = 10) and IUGR (n = 15) births by in-situ hybridization procedure. Their expression was also studied in first (n = 5) and second (n = 5) trimester placentae obtained from elective termination of normal pregnancies. Both IGF-I and PGH expression were found to be higher in the first and second trimester placentae compared to term placentae in normal pregnancies. However, IUGR term placentae showed increased expression of both IGF-I and PGH mRNA in comparison with normal placentae. Various mechanisms leading to the increased transcription of IGF-I and PGH mRNA in IUGR placenta are discussed. This increased transcription perhaps occurs in response to the reduction in the fetal growth.

P100IUGR fetuses with abnormal umbilical artery Doppler and elevated S100B protein levels

Maternal and umbilical blood samples were collected in IUGR pregnancies with abnormal umbilical artery Doppler findings and in controls. S100B protein levels were measured by means of a specific radioimmunoassay and flow velocimetry waveforms were recorded from uterine, umbilical and fetal middle cerebral arteries. We studied the correlation between S100B protein, an acidic calcium binding protein previously demonstrated as a reliable indicator of brain lesion, and the degree of fetoplacental blood flow impairment to examine whether S100B could be helpful in the detection of brain sufference in intrauterine growth retarded (IUGR) fetuses. Mean S100B protein in umbilical plasma were higher (P &lt; 0.05) in IUGR patients (113.5 ± 65.9 fmol/mL) than in controls (52.7 ± 34.8 fmol/mL), and particularly in those cases in which brain sparing was present (169.6 ± 67.8 fmol/mL). Fetal S100B concentrations were correlated with middle cerebral artery PI (r = −0.50, P &lt; 0.05) and with umbilical artery PI/middle cerebral artery PI ratio (r = 0.51, P &lt; 0.05). This study provides evidence that fetal S100B protein is increased in IUGR and suggests that it may play.

Effect of IGF‐I on placental thromboxane and prostacyclin release in severe intrauterine growth retardation

Our recent findings that IGF-I inhibits placental thromboxane (TxB2) release (1, 2) and that prostanoid release from placentas of certain pregnancies complicated by intrauterine growth retardation (IUGR) is decreased [Sorem KA, Siler-Khodr TM, Placenta, 16:503–515, 1995] led us to investigate the effect of IGF-I on prostanoid release from placentas of IUGR pregnancies. The placental response of 6-keto-prostaglandin F1a (6-keto-PGF1a) and thromboxane (TxB2) to IGF-I in severe IUGR (n = 5) was compared with the response in normal pregnancies (n = 6). Placentas were perifused with medium containing IGF-I at doses of 0, 5.2, 10.4, 20.8, and 83.3 ng/ml. In three of the five IUGR placentas (responsive group), incubation with IGF-I resulted in an inhibition of TxB2, attaining significantly greater inhibition at a lower dose of IGF-I than the normal placental response. However, in two of the five IUGR placentas (non-responsive group), the TxB2 was insensitive to the normal inhibitory action of IGF-I. The baseline production of prostanoids from the IUGR placentas was not predictive of their response to IGF-I. Moreover, 6-keto-PGF1a was not inhibited in any of the placentas, IUGRs, or normals. However, the ratio for TxB2 over 6-keto-PGF1a basal production rate from the zero treatment time to the fifth hour was significantly less in the nonresponsive IUGR placentas than for the responsive IUGR placentas or for the normal placentas. Certain IUGR placentas demonstrated a significant suppression of TxB2 with IGF-I, whereas other IUGR placentas were insensitive to exogenous IGF-I. A decreased and unchanging ratio of TxB2/6-keto-PGF1a production rate was characteristic of the nonresponders. J. Matern.-Fetal Med. 6: 341–350, 1997. © 1997 Wiley-Liss, Inc.

Effect of IGF-I on placental thromboxane and prostacyclin release in severe intrauterine growth retardation.

Our recent findings that IGF-I inhibits placental thromboxane (TxB2) release (1, 2) and that prostanoid release from placentas or certain pregnancies complicated by intrauterine growth retardation (IUGR) is decreased [Sorem KA, Siler-Khodr TM, Placenta, 16:503-515, 1995] led us to investigate the effect of IGF-I on prostanoid release from placentas of IUGR pregnancies. The placental response of 6-keto-prostaglandin F1a (6-keto-PGF1a) and thromboxane (TxB2) to IGF-I in severe IUGR (n = 5) was compared with the response in normal pregnancies (n = 6). Placentas were perifused with medium containing IGF-I at doses of 0, 5.2, 10.4, 20.8, and 83.3 ng/ml. In three of the five IUGR placentas (responsive group), incubation with IGF-I resulted in an inhibition of TxB2, attaining significantly greater inhibition at a lower dose of IGF-I than the normal placental response. However, in two of the five IUGR placentas (non-responsive group), the TxB2 was insensitive to the normal inhibitory action of IGF-I. The baseline production of prostanoids from the IUGR placentas was not predictive of their response to IGF-I. Moreover, 6-keto-PGF1a was not inhibited in any of the placentas, IUGRs, or normals. However, the ratio for TxB2 over 6-keto-PGF1a basal production rate from the zero treatment time to the fifth hour was significantly less in the nonresponsive IUGR placentas than for the responsive IUGR placentas or for the normal placentas. Certain IUGR placentas demonstrated a significant suppression of TxB2 with IGF-I, whereas other IUGR placentas were insensitive to exogenous IGF-I. A decreased and unchanging ratio of TxB2/6-keto-PGF1a production rate was characteristic of the nonresponders.

Effect of IGF-I on Placental Thromboxane and Prostacyclin Release in Severe Intrauterine Growth Retardation

Our recent findings that IGF-I inhibits placental thromboxane (TxB2) release (1,2) and that prostanoid release from placentas of certain pregnancies complicated by intrauterine growth retardation (IUGR) is decreased [Sorem KA, Siler-Khodr TM, Placenta, 16:503–515, 1995] led us to investigate the effect of IGF-I on prostanoid release from placentas of IUGR pregnancies. The placental response of 6-keto-prostaglandin F1a (6-keto-PGF1a) and thromboxane (TxB2) to IGF-I in severe IUGR (n = 5) was compared with the response in normal pregnancies (n = 6). Placentas were perifused with medium containing IGF-I at doses of 0, 5.2, 10.4, 20.8, and 83.3 ng/ml. In three of the five IUGR placentas (responsive group), incubation with IGF-I resulted in an inhibition of TxB2, attaining significantly greater inhibition at a lower dose of IGF-I than the normal placental response. However, in two of the five IUGR placentas (non-responsive group), the TxB2 was insensitive to the normal inhibitory action of IGF-I. The baseline production of prostanoids from the IUGR placentas was not predictive of their response to IGF-I. Moreover, 6-keto-PGF1a was not inhibited in any of the placentas, IUGRs, or normals. However, the ratio for TxB2 over 6-keto-PGF1a basal production rate from the zero treatment time to the fifth hour was significantly less in the nonresponsive IUGR placentas than for the responsive IUGR placentas or for the normal placentas. Certain IUGR placentas demonstrated a significant suppression of TxB2 with IGF-I, whereas other IUGR placentas were insensitive to exogenous IGF-I. A decreased and unchanging ratio of TxB2/6-keto-PGF1a production rate was characteristic of the nonresponders.