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PubMedDate not supplied

Changes in activity of enzymes related to glycolysis, gluconeogenesis and lipogenesis in placentae from diabetic women.

The activity of enzymes with a regulatory function in the pathways of glycolysis, gluconeogenesis and NADP-generation was investigated in 50 placentae from normal pregnancies and deliveries, 23 placentae from women with gestational diabetes, and 12 placentae from insulin-dependent patients. In placentae from the gestational diabetic group, the activity of pyruvate kinase and of NADPH-generating enzymes was raised and the activity of enzymes connected to glucogenesis was unchanged. These alterations were attributed to the oversupply of glucose and insulin to morphologically normal and well-oxygenated placental tissue. In the placentae from the insulin-dependent group, the activity of pyruvate kinase was reduced, the activity of NADPH-generating enzymes was enhanced and the activity of those related to the gluconeogenesis was unchanged. It is suggested that this pattern of enzyme changes reflects a reduction in the glycolytic capacity in these placentae, which may be due to inhibition by products of enhanced fatty acid oxidation in diabetes, amino acids and/or by long-term anoxia as a result of uteroplacental circulatory disturbances. The possible relation of reduced energy-forming capacity of the placenta in diabetes to its transport function is discussed.

Aspartate Aminotransferases↗
PubMedDate not supplied

High densities of angiotensin II subtype 2 (AT2) receptors in the porcine placenta and fetal membranes.

The present study was undertaken in order to characterize and determine angiotensin (Ang) II receptors and renin in the porcine placenta and fetal membranes. High densities of Ang II receptors of subtype 2 (AT2 receptors) were demonstrated in all parts of the placenta and fetal membranes throughout gestation. AT1 receptors (subtype 1) were only found in the first part of the gestation and only in the allantochorion-endometrium at low densities. The total Ang II receptor density was increased in the allantochorion-endometrium in the last stage of gestation. Except for this finding the Ang II receptor density did not vary during gestation. Some of the highest receptor densities were found in the allantoamnionic membrane. The Ang II receptor densities did not correlate with the duration of the gestation in any part of the placenta. Enzymatically active renin was found in all parts of the porcine placenta and fetal membranes in concentrations similar to those found earlier in the blood plasma. The renin concentrations did not correlate with the Ang II receptor densities or the duration of the gestation in any part of the placenta. Compared with the human placenta, where the Ang II receptors are almost exclusively AT1 receptors and low receptor densities are found in the fetal membranes, the present results indicate profound species differences in the expression and function of the renin-angiotensin system in the placenta and fetal membranes.

Angiotensin Receptor Antagonists↗
PubMed1996

Placenta morphology and absent or reversed end diastolic flow velocities in the umbilical artery: a clinical and morphometrical study.

The aim of the study was to investigate if a relation exists between absent or reversed end diastolic (ARED) flow in the umbilical artery and morphometric characteristics of the placenta. Geometric parameters were measured in the terminal villi of nine placentae, collected after a pregnancy complicated by ARED flow. Placentae from pregnancies with normal Doppler velocimetry in the umbilical artery were matched for gestational age and formed the control group. Mean placental weight in the ARED group was significantly lower than in the control group. Morphometric characteristics of the terminal placental villi did not differ substantially between the two groups before 30 weeks gestation. After 30 weeks mean villous profile cross sectional area and diameter were significantly smaller in the ARED group than in the control group. The mean profile cross sectional villous diameter in the ARED group did not differ substantially before and after 30 weeks of gestation (2287 microns2 and 2303 microns2, respectively). Accelerated maturation of terminal villi occurs in placentae delivered after a pregnancy with ARED flow in the umbilical artery. Morphometric characteristics are significantly different between placentae expelled after ARED velocities or after normal Doppler recordings in the umbilical artery. In ARED placentae, a significantly more uniform pattern of small villi is found compared with control placentae.

Blood Flow Velocity↗
PubMedDate not supplied

Fibroblast growth factor-2 and fibroblast growth factor receptor-1 mRNA expression and peptide localization in placentae from normal and diabetic pregnancies.

Fibroblast growth factor-2 (FGF-2) is a potent mitogen expressed widely during embryogenesis and in tissues of the human fetus. It is recognized as an endothelial cell mitogen and is angiogenic in vivo. Expression of FGF-2 mRNA has also been shown within the human term placenta, and FGF-2 isolated from placental tissue, suggesting a role in placental growth including angiogenesis. The purpose of this study was to quantify and localize the sites of expression of FGF-2 and its high-affinity receptor, FGFR1, within placentae from normal term human pregnancies (n=8, 39-42 weeks), and pregnancies complicated by pregestational, type 1 diabetes (n=8, 36-40 weeks). Tissues were collected immediately following delivery and were either snap-frozen for RNA isolation, or fixed for either in situ hybridization using a 35S-labelled cRNAs encoding human FGF-2 or FGFR1, or immunocytochemistry using antibodies against human FGF-2 or FGFR1. Northern blot hybridization showed a significantly increased abundance of mRNAs for both FGF-2 and FGFR1 in placentae from diabetic women compared to those from normal women. In normal term placenta FGF-2 mRNA was present at low abundance in fetal villous tissue, in the vascular endothelium of blood vessels, and in the syncytiotrophoblast. FGF-2 mRNA was considerably more abundant in the syncytiotrophoblast and villous tissue of placentae from diabetic patients. Messenger RNA for FGFR1 was similarly distributed to that encoding FGF-2. Immunocytochemistry revealed abundant FGF-2 and FGFR1 peptides in villous vascular endothelial cells, and associated with the cell membranes of stromal tissues in placentae from control pregnancies. Little immunoreactive FGF-2 was present in the syncytiotrophoblast at term. In pregnancies complicated by diabetes intense staining for immunoreactive FGF-2 and for FGFR1 additionally existed in syncytiotrophoblast. The results suggest that FGF-2 acting as an autocrine agent contributes to placental angiogenesis, but may be released from the syncytium into the maternal circulation. Expression is elevated in placentae from diabetic pregnancies, and is particularly associated with the syncytiotrophoblast. This suggests a placental source for the elevated circulating maternal FGF-2 previously described in diabetic pregnancy.

Adult↗
PubMed2003

Expression of angiopoietic factors in normal and type-I diabetes human placenta: a pilot study.

OBJECTIVES: Morphological changes of blood vessel wall have been described in placenta from pregnancies complicated by diabetes mellitus type-I. STUDY DESIGN: We measured mRNA expression of vascular endothelial growth factor (VEGF), angiopoietin 1 and 2 (Ang-1 and Ang-2), their receptors VEGFR-1, VEGFR-2, Tie-2, fibroblast growth factor 2 (FGF-2), and its receptor FGF-2R in placental tissue of diabetes type-I patients, in normal term placenta, and endometrium of non-pregnant women by real time reverse transcriptase PCR. RESULTS: The expression of Ang-2 and VEGFR-1 mRNAs was significantly higher in placenta (P<or=0.01). The expression of VEGF and VEGFR-2 mRNAs was significantly lower in normal term or diabetes type-I placenta compared to human endometrium (P<or=0.01). We did not detect a significant difference in the expression of Ang-1, Ang-2, Tie-2, VEGF, VEGFR-1, VEGFR-2, FGF-2, and FGF-2R in normal and diabetes type-I placenta. CONCLUSION: These data show differential expression of Ang-2, VEGFR-1, VEGF, and VEGFR-2 in placenta and endometrium. The expression of Ang-1, Ang-2, Tie-2, VEGF, VEGFR-1, VEGFR-2, FGF-2, and FGF-2R was not different in normal and type-I diabetes placenta.

Angiopoietin-1↗
PubMed1997

Muscarinic cholinergic receptor subtypes expression by human placenta.

The presence of a cholinergic system in the placenta is suggested by several data, but no information is available concerning cholinergic receptor expression by placenta. The present study was designed to investigate muscarinic cholinergic receptors in sections of human placenta using a radioligand binding techniques with [3H]N-methyl scopolamine ([3H]NMS) as a ligand. [3H]NMS was bound to sections of human placenta in a manner consistent with the labelling of muscarinic cholinergic receptors. The dissociation constant (Kd) value was 0.1 +/- 0.03 nM and the maximum density of binding site (Bmax) value was 10.82 +/- 0.09 fmol/mg of tissue. The binding was time-, temperature- and concentration-dependent, belonging to one class of high affinity sites. Analysis of [3H]NMS displacement curves by compounds acting on the different subtypes of muscarinic cholinergic receptor subtypes suggests that human placenta expresses the four subtypes (M1-M4) of muscarinic cholinergic receptor assayable with radioligand binding assay techniques. The demonstration of muscarinic cholinergic recognition sites in human placenta may contribute to define the possible significance of placental cholinergic system. Moreover, human placenta can be used as an easily obtainable human source of M1-M4 muscarinic cholinergic receptor subtypes.

Adult↗
PubMedDate not supplied

Developmental expression of vascular endothelial growth factor and its receptors in ovine placenta and fetal membranes.

OBJECTIVES: Vascularity of the surface of the placenta in humans and of the placenta and fetal membranes in several species including sheep is an important determinant of intramembranous absorption of amniotic fluid. Our previous studies have shown that the total blood vessel surface area in ovine amnion and chorion increases with advancing gestation. Vascular endothelial growth factor (VEGF) is a potent angiogenic and permeability factor and is found to be expressed in the ovine placenta and fetal membranes. To investigate the role of VEGF in maintaining the absorptive function of the intramembranous microvessels, the present study was undertaken to determine the gestational change in gene expression of VEGF and its receptors, kinase insert domain-containing receptor (KDR) and fms-like tyrosine kinase (Flt-1), in ovine placenta, chorion, and amnion. METHODS: Total RNA was extracted from placental cotyledon, chorion, and amnion of ovine fetuses at 60-140 days of gestation. The relative abundance of VEGF, KDR, and Flt-1 mRNA was determined by Northern blot analysis, and VEGF molecular forms expressed were identified by reverse transcriptase polymerase chain reaction. The gestational changes in mRNA levels of VEGF and its receptors were analyzed by regression analysis. RESULTS: In ovine placenta, chorion, and amnion, VEGF mRNA levels increased significantly from 60 to 140 days. The major VEGF molecular form expressed in these tissues was VEGF164, whereas VEGF120, VEGF144, and VEGF188 were present at lower levels. In the placenta, KDR was the primary VEGF receptor expressed, although Flt-1 was also detected at very low levels. In the amnion and chorion, KDR was the only receptor expressed. A gestational-dependent change in VEGF receptor expression was not observed in the placenta and membranes. CONCLUSIONS: The increase in VEGF gene expression with advancing gestation in the amnion and chorion where KDR is expressed suggests that VEGF and its receptor are important determinants of vascularity and permeability, and thus exchange capacity, of the intramembranous pathway.

Amnion↗
PubMed1999

3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and DNA incorporation in normal human placentas perfused with AZT.

Vertical transmission of the human immunodeficiency virus 1 (HIV-1) is reduced from approximately 25% to approximately 7% as a result of 3'-azido-3'-deoxythymidine (AZT) therapy given during pregnancy; however, the consequences of transplacental AZT exposure to the fetus remain unknown. To address the extent and kinetics of AZT transfer across the human placenta, perfusion studies have been performed with fresh uninfected human placentas perfused with 0.5, 1. 0 and 5.0 mg AZT/ml for 2 h using a dual recirculating single cotyledon perfusion apparatus [T.I. Ala-Kokko, P. Pienimaki, R. Herva, A.I. Hollmen, O. Pelkonen, K. Vähäkangas, Transfer of lidocaine and bupivacaine across the isolated perfused human placenta, Pharmacol. Toxicol. 77 (1995) 142-148]. For two placentas, samples of perfusion effluent were taken every 15 min from the maternal and fetal sides of the apparatus and AZT levels were determined by AZT radioimmunoassay (RIA). At the end of the perfusion, AZT-DNA incorporation into placental DNA was determined by AZT-RIA. The concentration of AZT in the fetal perfusate increased with time, along with a concomitant slow decrease in the concentration of AZT in the maternal perfusates. For three different placentas, at 2 h after the start of perfusion, AZT-DNA incorporation values (molecules of AZT/10(6) nucleotides) were 11.8 for the 0.5 mg AZT/ml perfusate, 13.7 for the 1.0 mg AZT/ml perfusion, and 42.0 for the 5 mg AZT/ml perfusion. An additional placenta perfused with 1 mg AZT/ml did not have detectable values of AZT incorporated into DNA (data not shown). The data show that AZT crosses the human placenta and becomes rapidly incorporated into DNA of placental tissue in a dose-dependent fashion, suggesting that even short exposures to this drug might induce fetal genotoxicity and might also inhibit maternal-fetal viral transmission.

Anti-HIV Agents↗
PubMed2001

Persistence of Plasmodium falciparum in the placenta after apparently effective quinidine/clindamycin therapy.

The persistence of Plasmodium falciparum in the placenta after apparently adequate therapy with quinine has been described. We describe this phenomenon in the placenta of a 19-year-old woman with falciparum malaria, who was treated with a combination of quinidine and clindamycin. Although this therapy was effective and diminished her peripheral blood parasitemia from 3% at presentation to almost undetectable at the time of delivery, vast numbers of P. falciparum-infected erythrocytes were present in the maternal sinusoids of the placenta. This sequestration of infected erythrocytes produced a local parasitemia in the placenta of 70% to 80%. Additionally, rare Plasmodium-infected erythrocytes were also seen in the fetal blood of the placenta. We review malaria in pregnancy, parasitic involvement of the placenta and emphasize that Plasmodium-infected erythrocytes may persist in the placenta even after clearance of parasites from the peripheral blood.

Adult↗
PubMed2003

Cotyledonary-like placenta associated with severe intrauterine growth restriction.

There have been no previous reports of human placentas mimicking the cotyledonary placenta of ruminants. We report a case of cotyledonary-like placenta associated with severe intrauterine growth restriction. A woman pregnant for the first time was referred to our hospital at 27 weeks' gestation because of severe intrauterine growth restriction. Characteristics of the placenta in the patient were examined by ultrasonographical and histopathological techniques. Ultrasonography revealed that a hypo-echoic area intermingled with small segmented tissues in the placenta. The hypo-echoic area changed in size and shape according to uterine contractions. At 31 weeks' gestation, a caesarean section was performed because of non-reassuring fetal status. A female baby weighing 814 g was delivered. The placenta, which weighed 260 g, contained several long stem villi running over a distance of 6 to 7 cm without branching into intermediate or terminal villi. Small villous tissues had developed only at the tips of these stem villi. The present case shows an extraordinarily abnormal development of the villous trees in the placenta, which may have caused fetal IUGR and non-reassuring fetal status.

Adult↗
PubMed1995

Transvaginal sonographic evaluation of first-trimester placenta previa.

Our objective was to determine the relationship between the placenta and the internal cervical os in the first trimester. This study included ultrasound examinations performed between 9 and 13 weeks' gestation over a 28-month period. The position of the lower edge of the placenta with respect to the internal cervical os was recorded for each transvaginal ultrasound examination. A total of 77 out of 1252 (6.2%) patients had a first-trimester placenta previa; four cases persisted until term. There were no false-negative diagnoses. Our conclusion is that approximately 6.2% of patients will have a placenta previa in the first trimester. Transvaginal sonography can exclude a diagnosis of placenta previa after 9 weeks' gestation. The likelihood that a placenta previa will persist until term increases if the placenta covers the internal cervical os by > or = 1.6 cm.

Female↗
PubMed2000

Human melanoma cells secrete and respond to placenta growth factor and vascular endothelial growth factor.

The vascular endothelial growth factor is produced by a large variety of human tumors, including melanoma, in which it appears to play an important role in the process of tumor-induced angiogenesis. Little information is available on the role of placenta growth factor, a member of the vascular endothelial growth factor family of cytokines, in tumor angiogenesis, even though placenta growth factor/vascular endothelial growth factor heterodimers have been recently isolated from tumor cells. To investigate the role of placenta growth factor and vascular endothelial growth factor homodimers and heterodimers in melanoma angiogenesis and growth, 19 human melanoma cell lines derived from primary or metastatic tumors were characterized for the expression of these cytokines and their receptors. Release of placenta growth factor and vascular endothelial growth factor polypeptides into the supernatant of human melanoma cells was demonstrated. Reverse transcriptase polymerase chain reaction analysis showed the presence of mRNAs encoding at least three different vascular endothelial growth factor isoforms (VEGF(121), VEGF(165), and VEGF(189)) and transcripts for two placenta growth factor isoforms (PlGF-1 and PlGF-2) in human melanoma cells. In addition, placenta growth factor expression in human melanoma in vivo was detected by immunohistochemical staining of tumor specimens. Both primary and metastatic melanoma cells were found to express the mRNAs encoding for vascular endothelial growth factor and placenta growth factor receptors (KDR, Flt-1, neuropilin-1, and neuropilin-2), and exposure of melanoma cells to these cytokines resulted in a specific proliferative response, supporting the hypothesis of a role of these angiogenic factors in melanoma growth. J Invest Dermatol 115:1000-1007 2000

Dimerization↗
PubMed2000

Effect of maternal cholestasis on bile acid transfer across the rat placenta-maternal liver tandem.

Cholestasis of pregnancy induces alterations in bile acid transport by human trophoblast plasma membrane (TPM) vesicles. We investigated whether maternal cholestasis affects the overall ability of the rat placenta to carry out vectorial bile acid transfer from the fetus to the mother. Complete obstructive cholestasis (OCP) was maintained during the last week of pregnancy and released at term (day 21), before experiments were performed. In situ single-pass perfusion of one placenta per rat with 250 nmol [(14)C]glycocholic acid (GC) revealed an impaired uptake in OCP rats (2.28 vs. 5.53 nmol in control rats). Approximately 100% of GC taken up by control placentas was secreted in maternal bile over 120 minutes (5.38 nmol), whereas this was only 61% (1.40 nmol) of the GC taken up by OCP placentas. When 5 nmol GC was administered through the jugular vein no significant difference between both groups in total GC bile output was found. The efficiency (V(max)/K(M)) of adenosine triphosphate (ATP)-dependent GC transport by vesicles from the maternal side of TPM was decreased (-41%) in OCP. Moreover, histological examination of the placentas suggested a reduction in the amount of functional trophoblast in the OCP group. This was consistent with a lower antipyrine diffusion across the placenta in these animals. In sum, our results indicate that maternal cholestasis affects the ability of the placenta to efficiently carry out bile acid transfer from fetal to maternal blood. Changes in both the structure and the functionality of the chorionic tissue may account for this impairment.

Animals↗
PubMed1999

Localization of thioredoxin reductase and thioredoxin in normal human placenta and their protective effect against oxidative stress.

Recent studies have indicated that oxidative stress is involved in the pathogenesis of pre-eclampsia. Oxidative stress damages systemic tissues, and placental damage may result in intrauterine growth retardation and fetal distress. Thus, this study attempted to elucidate the placental localization of thioredoxin and thioredoxin reductase, substances that may reduce oxidative stress. Furthermore, it studied the defence mechanism of the thioredoxin-thioredoxin reductase system against oxidative stress in mitochondria of normal human placenta where reactive oxygen species are primarily produced. The examination of thioredoxin reductase activity in subcellular fractions of human placenta indicated that thioredoxin reductase was located not only in cytoplasm, but also in mitochondria. The existence of thioredoxin and thioredoxin reductase in human placenta was confirmed immunologically using antibodies raised against thioredoxin and thioredoxin reductase. Thioredoxin and thioredoxin reductase were localized histochemically in cytotrophoblasts, decidua, and stromal cells in the stem villi. The addition of exogenous thioredoxin and thioredoxin reductase to fumarase in mitochondria of human placenta displayed a protective effect against oxidative stress. In conclusion, this study confirmed the intracellular localization and the tissue distribution of thioredoxin and thioredoxin reductase in human placenta. Moreover, the complete thioredoxin-thioredoxin reductase system in human placenta may protect the placenta from damage caused by oxidative stress.

Blotting, Western↗
PubMed1999

Expression of thioredoxin and thioredoxin reductase in placentae of pregnant mice exposed to lipopolysaccharide.

We have previously shown that thioredoxin and thioredoxin reductase were immunohistochemically localized in cytotrophoblasts, decidua and stromal cells in the stem villi of human placenta and that the addition of exogenous thioredoxin and thioredoxin reductase to mitochondrial fractions from human placenta displayed a protective effect on fumarase activity against oxidative stress. In this study, to investigate further the roles of thioredoxin and thioredoxin reductase in protecting pregnancy against oxidative stress, we examined the effect of lipopolysaccharide (LPS), which induces a variety of cytokines and produces radical oxygen species, on the expression of thioredoxin and thioredoxin reductase in mouse placenta. We focused on the placental protective effect in the second trimester, when the onset of placental dysfunction might occasionally lead to a critical state for the fetus. Thus we analysed placentae from mice on day 13 of pregnancy at various time points after they were injected with LPS (50 microg/kg i.p.) or saline as a control. The expressions of thioredoxin and thioredoxin reductase were evaluated by Western blotting and immunohistochemistry. Western blot analysis revealed that LPS approximately quadrupled the expression of both thioredoxin and thioredoxin reductase in the placentae of pregnant mice. When both proteins were localized immunohistochemically, it was found that the decidua and the diploid trophoblasts in the basal zone were intensively stained. Furthermore, the expression of 4-hydroxy-2-nonenal (HNE)-modified proteins, which are markers of oxidative stress, was enhanced in placenta by LPS. Our study suggests that the induced thioredoxin and thioredoxin reductase might protect the placenta from the stress induced by LPS.

Aldehydes↗
PubMed2000

Fatty acid transport regulatory proteins in the developing rat placenta and in trophoblast cell culture models.

The placenta forms a selective barrier that is able to transport nutrients that are of critical use to the fetus. Delivery of essential fatty acids to the fetus is dependent upon transplacental transport and provides the backbone for the biosynthesis of biological membranes, myelin and various signalling molecules. The primary objective of this research was to elucidate the expression patterns of genes that regulate fatty acid transport across the placenta. Several fatty acid transport regulatory genes have been identified in the rat including; cytoplasmic heart fatty acid binding protein (hFABP), plasma membrane fatty acid binding protein (FABPpm), fatty acid translocase (FAT) and fatty acid transport protein (FATP). In this study, we have elucidated temporal and spatial expression patterns for these genes in the rat placenta and in cell culture models of the rat placenta by Northern blot, RT-PCR, Western blot and/or by in situ hybridization analyses. Expression of hFABP was specific to the labyrinth zone, the main barrier and site of transplacental transport in the rat placenta. In addition, the levels of hFABP expression increased with gestational age, suggesting a growing requirement for fatty acid transport with advancing stages of pregnancy. FABPpm, FAT and FATP are expressed in both the junctional and labyrinth zones of the rat placenta. FAT was predominantly localized to the labyrinth zone by in situ hybridization analysis. The placental cell expression patterns of the genes involved in fatty acid transport were supported by our observations of HRP-1 (labyrinth zone) and Rcho-1 (junctional zone) trophoblast cell culture models. Given their cell surface location, we predict that FABPpm, FAT and FATP potentially participate in placental fatty acid uptake. The predominant expression of hFABP and FAT in the labyrinth zone of the chorioallantoic placenta implicates hFABP and FAT in the transplacental movement of fatty acids from maternal to fetal compartments.

Animals↗
PubMed2001

Expression of intercellular adhesion molecule 1 (ICAM-1) in Plasmodium falciparum-infected placenta.

We investigated the expression of intercellular adhesion molecule 1 (ICAM-1) in malarial placenta and related histological changes. Thirty-two malarial and 40 control term placentae were collected at Tanga, Tanzania and examined histologically and immunohistochemically. Malaria infected placentae were further divided into acute (15) and chronic (17) cases according to the presence of malarial pigment. The expression of ICAM-1 on monocyte, syncytio- and cytotrophoblasts, endothelial and stromal cells was assessed. Birthweight was lower and leukocyte counts higher in placentae with chronic infection. Many monocytes were present within the intervillous spaces, especially in placentae with chronic infection, and aggregated with parasitized erythrocytes. Some monocytes were adhesive to the surface of fibrinoid deposits. ICAM-1 expression on monocytes of malarial placentae was significantly conspicuous and correlated to the degree of intervillous leukocyte infiltration. Syncytiotrophoblasts often did not show ICAM-1, even though ICAM-1 was expressed by endothelium and weakly by cytotrophoblasts and stromal cells in both infected and control placentae. These results suggest that the expression of ICAM-1 on monocytes contributes to sequestration of infected erythrocytes within the intervillous spaces and their adhesion to fibrin masses and that ICAM-1 is unlikely to be associated with the direct adhesion of infected erythrocytes to the syncytiotrophoblasts.

Birth Weight↗
PubMed1991

A prostacyclin analogue crosses the in vitro perfused human placenta and improves transfer in some pathologic states.

Placental blood flow is reduced in pregnancies complicated by hypertension, intrauterine growth retardation, maternal smoking, or diabetes. Umbilical-placental production of the potent vasodilator prostacyclin is also reduced in these pathologic states and this deficiency may contribute to an associated increase in the incidence of low infant birthweight by affecting a reduction in placental nutrient transfer. We have studied the effects of the prostacyclin analogue carbacyclin on diffusional transfer in the human placenta perfused in vitro. We have found that carbacyclin crosses the human placenta and can significantly increase diffusional transfer in placenta from pregnancies complicated by hypertension or maternal smoking and in the normal term placenta in which prostacyclin production has first been reduced through the administration of ibuprofen. Carbacyclin had no effect, however, in untreated placenta from normal pregnancies or in placenta from diabetic pregnancies. These results suggest that the prostacyclin-deficient perfused placenta may serve as a model for several placental insufficiency syndromes and that the possibility that prostacyclin analogues may improve deficient nutrient transfer in some pathologic pregnancies warrants further investigation.

Antipyrine↗