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Pituitary adenylate cyclase-activating polypeptide (PACAP) and PACAP-receptor type 1 expression in rat and human placenta.

Pituitary adenylate cyclase-activating polypeptide (PACAP), the new hypophysiotropic factor member of the vasoactive intestinal peptide (VIP)/secretin/glucagon/GHRH family of neuropeptides, exerts its biological action by interacting with both PACAP-selective type I receptors (PAC1) and type II receptors (VPAC1), which bind both PACAP and VIP. The placenta is a site of production of hypophysiotropic factors that participate in the control of local hormone production, as well as the respective hypothalamic-pituitary neurohormones. In the present study, we show the expression of PACAP gene and irPACAP distribution within rat and human placental tissues, by means of RT-PCR and immunohystochemical experiments. In both rat and human placenta, we evaluated the expression of PAC1 gene by Northern hybridization analysis performed with a 32P-labeled 706 nt complementary DNA probe, derived from the full-length coding region of the rPAC1 complementary DNA. The results of these experiments demonstrate the presence, in both human and rat placenta, of a 7.5-kb transcript similar in size to those detected in the ovary, brain, and hypothalamus. Alternative splicing of two exons occurs in human and rat PAC1 gene generating splice variants with variable tissue-specific expression. To ascertain which of the splice variants were expressed in placental tissue we performed RT-nested PCR using primers flanking the insertion sequence termed hip/hop cassette in rat or SV1/SV2 box in human gene. Electrophoretic analysis of the PCR products showed a different pattern of expression of messenger RNA splicing variants in human and rat placenta. In particular, the rat placenta expresses the short PAC1 receptor (PAC1short), the rPAC1-hip or hop (which are indistinguishable with the primers used), and the rPAC1-hip-hop, whereas the human placenta expresses only the PAC1SV1 (or SV2) variant, structurally homologous to the rat PAC1 hip (or hop). Sequence analysis of the human PCR-amplified PAC1 variant was therefore carried out and revealed that human placenta only expresses the PAC1SV2 isoform. The presence and characterization of PACAP binding sites was then investigated in human placenta by radioligand binding studies performed on crude membrane preparation using [125I]PACAP27 as tracer. Scatchard analysis of the binding results revealed the presence of two binding sites, one with high affinity and low capacity (Kd 0.33+/-0.04 nM; Bmax 36.9+/-12.1 fmol/mg protein) and one with low affinity and high capacity (Kd 24+/-6.9 nM, Bmax 9.3+/-0.19 pmol/mg protein). The relative potencies of PACAP-related peptides for inhibition ofradioligand binding were: PACAP27 > or = PACAP38 > VIP, whereas GHRH and other unrelated peptides, such as CRH and beta-endorphin, did not inhibit [125I]PACAP27 binding. In conclusion, in this study, we provide evidence for the expression of PACAP within rat and human placenta. We also demonstrate that both human and rat placenta express the PAC1 gene and that the human tissue has binding sites for PACAP. These findings may suggest a role for PACAP in the regulation of placental physiology through autocrine and/or paracrine mechanisms.

Animals↗

Low serine hydroxymethyltransferase activity in the human placenta has important implications for fetal glycine supply.

Glycine is essential for fetal development, but in both sheep and human pregnancy, little is transported directly from the mother to the fetus, indicating that fetal glycine is derived from other sources. In the sheep, placental conversion of maternal serine by serine hydroxymethyltransferase (SHMT) provides almost all the glycine transported to the fetus. Although mRNA for mitochondrial and cytoplasmic SHMT has been detected in human placenta, it is not known whether substantial placental conversion of serine to glycine occurs in species other than sheep. We determined SHMT activity in human, rat, and sheep placenta by measuring conversion of [3-(14)C]serine to (14)C-methylene tetrahydrofolate. Compared with term human placenta, SHMT activity per gram of placenta was 5.1-fold higher in term rat placenta and 24.1-fold higher in term sheep placenta. In sheep placenta, SHMT activity per gram of placenta increased 2.1-fold between mid-gestation and term. In human placenta, placental SHMT activity was similar 8 wk post conception and at term. The low activity of SHMT in the human and rat placenta suggests that, unlike in the sheep, placental conversion of serine to glycine is not a major source of fetal glycine in these species.

Animals↗

Expression of inflammatory cytokines in placentas from women with preeclampsia.

It is postulated that inadequate remodeling of the uterine spiral arteries in preeclampsia leads to focal ischemia and generation of inflammatory cytokines, such as tumor necrosis factor (TNF alpha) and interleukins (ILs), by the placenta. Our objective was to compare TNF alpha, IL-1 alpha, IL-1 beta, and IL-6 levels in placentas from patients with preeclampsia and normal term pregnancies. Because the placenta is a large heterogeneous organ, we analyzed multiple sites per placenta. On the average, there was a 3-fold variation in cytokine protein levels across the eight sites analyzed for each placenta. However, there were no significant overall differences among the normal term, preeclamptic, and preterm placentas from women without preeclampsia. There were also no significant differences in TNF alpha messenger ribonucleic acid between the normal term and preeclamptic placentas, although TNF alpha messenger ribonucleic acid levels were lower in placentas from preterm patients without diagnosis of preeclampsia than in the normal term placentas. In vitro, hypoxia stimulated the production of TNF alpha, IL-1 alpha and IL-1 beta, but not that of IL-6, by placental villous explants from both groups of patients, and this was not exaggerated in preeclampsia. Finally, although peripheral and uterine venous levels of TNF alpha were elevated in preeclamptic women compared with normal term patients, the ratio of uterine to peripheral venous TNF alpha levels was not significantly different from 1.0 for either patient group. Taken together, these results suggest that sources other than the placenta contribute to the elevated concentrations of TNF alpha and IL-6 found in the circulation of preeclamptic women.

Culture Techniques↗

Comparative study on the expression of cytokine--receptor genes in normal and preeclamptic human placentas using DNA microarrays.

AIMS: To study the relationship between the expression levels of cytokine/receptor genes in placenta and the pathogenesis of pre-eclampsia. METHODS: The study was performed to compare the mRNA contents of cytokine (receptor) superfamily genes in placentas from 5 patients with pre-eclampsia and 5 strictly matched normal pregnancies. A complementary DNA microarray representing over 220 cytokine-associated genes was employed to complete the detection. RESULTS: It was shown that, among the 221 kinds of cytokine-associated genes, 162 of those including 22 interleukin/interleukin receptor genes presented with a difference of over two times in pre-eclamptic placentas compared to normal placentas. Most of the 22 interleukin/interleukin receptor genes were shown to be highly expressed in preeclamptic placenta, while the expression of IL-2 receptor (IL-2 R alpha, GenBank: X01057) gene in preeclamptic placenta was comparatively lower than that in normal placenta. Furthermore, some tumor necrosis factor (TNF)/receptor superfamily genes, including TNF (GenBank: X02910), TNF ligands (GenBank: U03398, U37518, AF053712, AF055872) and TNF receptors (GenBank: X60592, X63717, M83554, AF016266, AF016267, U81232) were also shown to be highly expressed in pre-eclamptic placenta. Besides interleukin and tumor necrosis factor (receptor) gene superfamily, the mRNA levels of another 39 cytokine and 15 cytokine receptor genes showed a two-fold difference between pre-eclamptic and normal placental tissues. Additionally, most of the genes were up-regulated in pre-eclamptic placenta. CONCLUSIONS: The up-regulation of cytokine-associated genes including interleukin and TNF (receptor) superfamily expression in placenta might be intensively related to the pathogenesis of pre-eclampsia.

Adult↗

DNA microarrays detect the expression of apoptosis-related genes in preeclamptic placentas.

AIMS: To investigate the expression of apoptosis-related genes in preeclamptic placentas and the possible mechanism of the regulation process. METHODS: Complementary DNA microarrays were employed to compare gene expression profiles of five preeclamptic and five normal placentas. RESULTS: Among the 368 genes detected over 35% showed an over 2-fold difference of expression between preeclamptic placentas and normal placentas. Many genes involved in cell cycle or apoptosis were more highly expressed in preeclamptic placentas than in normal placentas. The expression of many immune-activation genes in preeclamptic placentas was also higher than that in normal placentas. Additionally, many cytokine receptor/kinase genes were also induced in preeclamptic placentas. CONCLUSIONS: The change in expression of cell apoptosis-related genes in placentas might be involved in the pathogenesis of preeclampsia, while the activation of the immune system might be one cause of this change.

Adult↗

HCS-HCG regulation in cultured placenta.

Tissue culture has been used to study the action of different substrates on the secretion of HCG and HCS in human placental explants. The following compounds have been studied: prostaglandins E2 and F2alpha, adrenaline and noradrenaline, oestriol and progesterone, glucose concentration. The investigators first measured the normal secretion of three term placentas and 2 months placentas. The activity of the compounds tested is expressed in per cent of the normal values. The investigators have checked that the cultivated cells were always viable by measuring the oxygen consumption during all the experiments. PG E2 and F2alpha are without action on term placentas. Adrenaline and noradrenaline reduce significantly the secretion HCS by full term placentas and have no action on HCG secretion. Oestriol always stimulates HCS secretion by full term placentas and 2 months old placentas, whereas progesterone stimulates young placentas and inhibits full term placentas. Both steroids have no action on HCG secretion. Glucose is essential for HCS secretion by placentas but high values of glucose in the medium signficantly reduce the HCS secretion by full term placentas.

Cells, Cultured↗

Preferential increase in prostaglandin endoperoxide H synthase compared with lipoxygenase activity in sheep placenta and amnion at term pregnancy and after intrafetal glucocorticoid administration.

Prostaglandins (PGs) have been implicated as stimulants to myometrial contractility at parturition in many species. To determine whether the increased production of PGs at parturition reflects a general increase in the metabolism of arachidonic acid or a specific increase in PG endoperoxide H synthase (PGHS) compared with lipoxygenase activities, and to determine intrauterine sites of these activities, we examined the metabolism of [3H]arachidonic acid by homogenates of placenta, amnion and chorion from sheep at days 78-80, 100-105, 135-140 of pregnancy and at term (day 145). Tissues were also obtained from fetuses at day 125; four of these were infused for 84 h with cortisol and four were used as saline-treated controls. The endogenous arachidonic acid content at the start of incubation was measured by capillary gas chromatography. Radioactive metabolites were separated and quantified by reverse-phase high-pressure liquid chromatography. At each gestational age arachidonic acid was converted to PGs, leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs). Conversion to PGs was greater in amnion than in chorion or placenta between days 78 and 140. The formation of PGs rose in placenta at term to a mean value twice that of amnion and ten times that of chorion. In amnion, the ratio of PG:LT rose significantly at term relative to 100-140 days of gestation. In placenta, the ratio of PG:LT produced from arachidonic acid and the ratio of total PGHS:lipoxygenase products rose significantly at term. In the day-125 fetuses treated with cortisol there was a significant increase in PG production relative to that in control fetuses infused with saline in placenta, amnion and chorion; the placenta and amnion being the major sites of PG production. Production of LTs and HETEs also rose significantly in the chorion and the placenta relative to controls. In both the placenta and the amnion there was a significant increase in the ratio of total PGHS to lipoxygenase products formed. We conclude that at term labour and in labour induced by intrafetal cortisol infusion, the placenta is the major site of arachidonic acid metabolism, and that there is a preferential increase in the formation of PGs over lipoxygenase products. These results are consistent with the suggestion that there is an increase in the expression or activity of PGHS in the placenta of sheep in late pregnancy.

Amnion↗

Monocarboxylate transporter 8 expression in the human placenta: the effects of severe intrauterine growth restriction.

Thyroid hormones (THs) are essential for normal fetal development, with even mild perturbation in maternal thyroid status in early pregnancy being associated with neurodevelopmental delay in children. Transplacental transfer of maternal THs is critical, with increasing evidence suggesting a role for 3,3',5-tri-iodothyronine (T3) in development and function of the placenta itself, as well as in development of the central nervous and other organ systems. Intrauterine growth restriction (IUGR) is associated with fetal hypothyroxinaemia, a factor that may contribute to neurodevelopmental delay. The recent description of monocarboxylate transporter 8 (MCT8) as a powerful and specific TH membrane transporter, and the association of MCT8 mutations with profound neurodevelopmental delay, led us to explore MCT8 expression in placenta. We describe the expression of MCT8 in normal human placenta throughout gestation, and in normal third-trimester placenta compared with that associated with IUGR using quantitative reverse transcriptase PCR. MCT8 mRNA was detected in placenta from early first trimester, with a significant increase with advancing gestation (P=0.007). In the early third trimester, MCT8 mRNA was increased in IUGR placenta compared with normal samples matched for gestational age (P<0.05), but there was no difference between IUGR and normal placenta in the late third trimester. Western immunoblotting findings in IUGR and normal placentae were in accord with mRNA data. MCT8 immunostaining was demonstrated in villous cytotrophoblast and syncytiotrophoblast as well as extravillous trophoblast cells from the first trimester onwards with increasingly widespread immunoreactivity seen with advancing gestation. In conclusion, expression of MCT8 in placenta from early gestation is compatible with an important role in TH transport during fetal development and a specific role in placental development. Altered expression in placenta associated with IUGR may reflect a compensatory mechanism attempting to increase T3 uptake by trophoblast cells.

Adult↗

Fine structural abnormalities of the placenta in diabetic rats.

In the streptozocin-induced diabetic rat, the placenta is larger and the fetus is smaller than normal. To study cellular differences that might contribute to the size and functional disparity between diabetic and control placentas, a light- and electron-microscopic analysis was performed on 14-, 18-, and 22-day (term) control and diabetic placentas. Diabetic placentas, especially later in gestation, were marked by the presence of large numbers of glycogen-distended cells in the basal zone. Within the placental labyrinth, the trophoblastic layers of the interhemal membrane were significantly thicker in the diabetic placentas on days 18 and 22, and large accumulations of liid droplets were present, especially in the inner two trophoblastic layers. In normal placentas there is a marked thinning of the placental barrier in the labyrinth by day 22 of gestation, making the thickness of the labyrinthine layers in age-matched diabetic placentas even more impressive. Finally, the labyrinth of 22-day diabetic placentas contained more glycogen and rough endoplasmic reticulum in the inner trophoblastic layer, a feature that is found in less-mature (18-day) control placentas. Thus, the diabetic placentas have a number of features that are consistent with functional immaturity/dysmaturity. Cytologic evidence confirms the presence of increased glycogen and lipid reserves in both the junctional zone and the cellular area between maternal and fetal blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Study on hepatitis B virus infection status in placentas of hepatitis B surface antigen positive pregnant women during middle and late period of pregnancy].

OBJECTIVE: To investigate Hepatitis B Virus (HBV) infection status in placentas of Hepatitis B Surface Antigen (HBsAg) positive pregnant women during middle and late period of pregnancy. METHODS: One hundred and sixty-seven placentas from HBsAg positive pregnant women were collected, including 158 term placentas and 9 aborted second-trimester placentas. HBsAg and hepatitis B core antibody (HBcAg) in placental cytotypes were detected by immunohistochemistry. RESULTS: Of the 158 term placentas, HBV infection rates in decidual cells (DC), trophoblastic cells (TC), villous mesenchymal cells (VMC) and villous capillary endothelial cells (VCEC) were 66.46% (105/158), 58.23% (92/158), 27.22% (43/158) and 12.66% (20/158), respectively. The HBV infection rates gradually decreased from maternal side to fetal side of placentas. Both HBsAg and HBcAg were mainly located in the cytoplasm of infected cells. The positive cells were mostly in focal distribution. One out of 9 aborted second-trimester placentas was infected. CONCLUSIONS: HBV infection was found in different cells of term placentas. The positive rates for HBsAg and HBcAg in placentas were gradually decreased from maternal side to fetal side. The positive rate was low in aborted second-trimester placentas.

Adult↗

[Hematopoietic stem/progenitor cells and phenotypes of lymphocyte subpopulations in human placenta].

OBJECTIVE: To study whether human placenta contains hematopoietic stem/progenitor cells (HSPCs), and analyze phenotypes of lymphocyte subpopulations in the placenta. METHODS: Nucleated cells from fresh human placenta were analyzed for phenotypes of HSPCs and lymphocyte subpopulations by flow cytometry (FCM). And CD(34)(+) cells were sorted from human placenta nucleated cells by FCM or MiniMACS. RESULTS: (1) CD(34)(+) cells, CD(34)(+)/CD(38)(+) cells, and CD(34)(+)/CD(38)(-) cells from a human placenta were 8.8, 4.6 and 11.9 times higher than those from umbilical cord blood (UCB), respectively. (2) The yields and purity of CD(34)(+) cells isolated from human placenta by FCM sorting system were (63.05 +/- 10.14)% and (86.39 +/- 11.27)%, respectively. (3) Lymphocytes, T cells (CD(3)(+)/CD(2)(+)), B cells (CD(19)(+)), Th cells (CD(3)(+), CD(4)(+)), and Th/Ts ratio in the placenta tissue were apparently lower than those in the UCB, while the CD(8)(+)/CD(28)(-) T suppressor cells were higher in the placenta than in the UCB. CONCLUSIONS: Human placenta is rich in HSPCs, and has important hematopoietic function in ontogeny. It is probable that human placenta would be graft resource for HSPCs transplantation. CD(8)(+)/CD(28)(-) T suppressor cells might play an important role in feto-maternal immunologic tolerance.

Cells, Cultured↗

Pathological changes in placentas from pregnancies with preeclampsia and eclampsia with emphasis on persistence of endovascular trophoblastic plugs.

AIM: To assess the frequency and types of histopathological changes in placentas from pregnancies complicated by preeclampsia/eclampsia. METHODS: Placentas routinely sent for pathological examination (n=1,689) were studied microscopically and compared to findings of 50 placentas from uncomplicated pregnancies. RESULTS: Out of 1,689 placentas from singleton pregnancies, 279 (16.5%) were from pregnancies complicated by preeclampsia/eclampsia. Seventy five placentas (26.8%) were appropriate for gestational age; other findings included: infarcts of various stage and volume in 63 cases (22.6%), minimal hypoxic damage in 27 cases (9.7%), accelerated maturation in 42 cases (15.1%), chronic villitis in 18 cases (6.5%), mixed findings in 18 cases (6.5%), intervillous thrombosis in 15 cases (5.4%), sub-choral thrombosis in 9 cases (3.2%), immaturity of the villi in 6 cases (2.1%), and findings suggestive of placental insufficiency in 6 cases (2.1%). Normal findings were significantly more frequent in the control group (P<0.001), but no other significant differences between the groups were found. In 4 (1.4%) placentas from pregnancies complicated by preeclampsia/eclampsia (gestational age 32 to 36 weeks), remnants of endovascular trophoblastic plugs in the vessels of the basal decidua were found. CONCLUSION: No significant difference was found between the group of placentas from pregnancies complicated with preeclampsia/eclampsia and the control group with regard to ischemic changes of the placenta. Endovascular trophoblastic plugs in the basal plate vessels from the third trimester placentas may play an additional role in the development of ischemic lesions in the placentas from pregnancies complicated with preeclampsia/eclampsia, but may also simply represent indirect evidence of the abnormal expression of certain adhesion molecules in this disorder.

Case-Control Studies↗

The placenta as a determinant of fetal well-being in normal and abnormal equine pregnancies.

One hundred twenty-four horse placentas were evaluated according to gross appearance, weight and surface area. Grossly abnormal placentas were photographed, and histological sections were taken from abnormal appearing areas, and from representative areas (pregnant horn, non-pregnant horn, body and cervical pole) in both normal and abnormal placentas. Information about the resulting foals was obtained and correlations examined. Histological sections were reviewed and related to the resulting foals. Four normal fresh placentas were infused with dyes to ascertain the blood supply to various areas. Foal weight was statistically related to both allantochorionic surface area and allantochorionic weight. When normal placental surface area was divided by foal weight and related to gestational age, a statistical (P less than 0.0001 and r = 0.829) relationship emerged. Long cords were seen frequently with fetal demise. Histological abnormalities in the placenta were highly associated with fetal demise or fetal abnormalities, with only 2 normal Thoroughbred foals resulted from the 23 placentas exhibiting abnormal histology. Among the ponies, the same relationship held, with 3 normal ponies delivered from 9 abnormal placentas. Normal placentas were associated with normal offspring in most cases. Perfusion studies indicated that, in the four placentas studied, one umbilical artery supplied the cervical area and the non-pregnant horn, whereas the other supplied the pregnant horn. The body had a mixed supply from both arteries. This study evaluated the feto-placental unit in terms of normal and abnormal measurements and histology related to foal outcome. The presence of abnormal histological appearance of the placenta appeared to be more closely associated with foal abnormality than the percentage of placental area involved in the abnormal process. More information is needed before placental blood supply can be related to abnormal processes.

Animals↗

[Do pregnant women with a low-situated placenta in the 16th week constitute a risk group?].

The object of this investigation was to elucidate whether pregnant women with low-placed placentae in the 16th week of pregnancy had more frequent haemorrhagic complications during pregnancy or during delivery and to demonstrate how many had placenta praevia at the time of delivery. In addition, the frequency of Caesarean section, the perinatal mortality, birthweights under 2,500 g in the infants delivered and placental anomalies were registered. A total of 1,572 pregnancies were investigated sonographically at about the 16th week of pregnancy and in 166 (10.6%) the placenta was found in the lower uterine segment. 40% of the 15 women with complete placenta praevia at the 16th week of pregnancy developed haemorrhage necessitating hospitalization, 27% were delivered by Caesarean section and 20% had placenta praevia at delivery. Out of 99 women with partial placenta praevia at the 16th week of pregnancy, one was found to have placenta praevia at the time of delivery but no significantly increased risk of haemorrhage necessitating hospitalization, abortion or Caesarean section. In 52 women with "deep insertion" of the placenta at the 16th week of pregnancy, one was subsequently found to have complete placenta praevia but the frequency of complications was not increased as compared with that in women with a free orifice. This investigation reveals a basis for control sonography of women with complete placenta praevia at the 16th week of pregnancy.

Female↗

Progesterone and estradiol production by normal and preeclamptic placentas.

Placentas obtained from women with preeclampsia produce more thromboxane, a potent vasoconstrictor, and less prostacyclin, a potent vasodilator, than normal. Although the factors responsible for this are not known, steroids are known to affect eicosanoid production, and the placenta is a rich source of progesterone and estradiol. If placental steroids contribute to the imbalance of increased thromboxane/decreased prostacyclin in preeclamptic placentas, then their placental production might also be abnormal. The following study was performed to see whether the placentas of preeclamptic women produce progesterone or estradiol abnormally. Fresh human term placentas were obtained immediately after delivery from normal and mild preeclamptic pregnancies. Whole placental tissues (350 mg) were incubated for three hours. Samples were collected and analyzed for progesterone and estradiol-17 beta by radioimmunoassay. Progesterone production was significantly higher in preeclamptic than in normal placentas without the addition of a precursor and with the addition of pregnenolone sulfate as a precursor, but not with the addition of pregnenolone alone. Both normal and preeclamptic placentas converted pregnenolone sulfate into progesterone as efficiently as they converted pregnenolone into progesterone. Estradiol production rates were similar in both preeclamptic and normal placentas, regardless of whether dehydroepiandrosterone sulfate was added as a precursor. These data indicate that placentas of women with mild preeclampsia produce more progesterone than normal, probably because they contain more pregnenolone sulfatase and larger stores of endogenous cholesterol. Higher concentrations of progesterone in the preeclamptic placenta could contribute to lower prostacyclin production because progesterone inhibits placental prostacyclin production.

Dehydroepiandrosterone↗

Fetal umbilical velocimetry for the surveillance of pregnancies complicated by placenta previa.

Continuous-wave Doppler studies of the umbilical arteries were performed on 100 women with placenta previa prior to delivery in the third trimester and 100 control subjects matched for gestational age and with normally implanted placentas. The ratio of the maximum (systole [S]) and minimum (diastole [D]) velocities appeared to reflect downstream vascular resistance. An S:D ratio of greater than or equal to 3.0 indicated elevation. There was a statistically higher S:D ratio in the placenta previa group as compared to the control group, and that difference persisted even when growth-retarded fetuses were excluded from both groups. Placenta previa patients with S:D ratios greater than or equal to 3.0 were associated with a statistically higher incidence of adverse pregnancy outcomes. The sensitivity, specificity, and positive and negative predictive value of an elevated S:D ratio in predicting adverse pregnancy outcomes were 90.0%, 93.8%, 62.0% and 98.5%, respectively. Our data suggest that (1) placenta previa patients are at increased risk of intrauterine growth retardation and adverse pregnancy outcomes, (2) placenta previa patients with normal S:D ratios are at no greater risk of adverse outcomes than are controls, (3) when the S:D ratio is elevated in placenta previa patients, it is more likely to be associated with adverse pregnancy outcomes, and (4) placenta previa patients without growth failure have a higher S:D ratio than do those with normally implanted placentas. Umbilical artery velocimetry appears to be a useful adjunct to ultrasound in the surveillance of pregnancies complicated by placenta previa.

Adult↗

[Glycogen-containing cells in the maternal and embryonic portions of the placenta in the rat and the common vole Microtus subarvalis].

Differentiation sequences and further transfiguration of glycogen-rich cells during placenta development were investigated for the rat and field vole Microtus subarvalis (11-20 day gestation). The presence of glycogen is a characteristic feature of decidual cells located in the region of lateral sinusoids, as well as of metrial gland cells, secondary giant trophoblast cells and trophoblast cells in the connective zone of placenta. Glycogen-containing metrial gland cells and trophoblast cells of connective zone of placenta are found to underlie the layer of tertiary giant trophoblast cells that cover the wall of the central arteria. Thus, both maternal and embryo-derived glycogen-containing cells always accompany the tertiary giant trophoblast cells that penetrate deeply into the maternal part of placenta but do not contain glycogen. In the field vole placenta the cells of peripheral trophoblast subpopulation of the connective zone of placenta attaching to the decidua basalis are stained by PAS-reaction more intensely than deeply situated ones. These data, as well as other phenomena revealed here, show that maternal and trophoblastic cells attaching to each other in placenta contain, as a rule glycogen. Glycogen cells in rat placenta and trophoblast cells of peripheral subpopulation of connective zone of placenta are similar in many respects. In this connection, a possible protective role of glycogen-containing cells, that probably favour the co-existence of maternal and embryo-derived cells in placenta, is discussed.

Animals↗

Abruptio placentae: perinatal outcome in normotensive and hypertensive patients.

OBJECTIVE: The objective of this study was to compare perinatal outcomes of hypertensive and normotensive women experiencing abruptio placentae. Our hypothesis is that hypertensive women have a less favorable perinatal outcome than do normotensive women. STUDY DESIGN: Women with the diagnosis of abruptio placentae delivered between July 1, 1988, and May 31, 1992, composed the study group (n = 226) in this case-control study. The incidence of abruptio placentae was 0.7% during this time. Those women with either multifetal gestations (n = 4) or delivery before 20 weeks' gestation (n = 2) were excluded from data analysis. The remaining 220 patients were divided according to their hypertensive (n = 29) or normotensive (n = 191) status. Maternal and neonatal medical records were reviewed and abstracted for demographic variables, antepartum complications, delivery route, abruptio placentae grade, neonatal gender, birth weight, Apgar score, cord pH, and perinatal mortality. These perinatal outcome variables were compared between the hypertensive and normotensive patient groups. RESULTS: Black women with abruptio placentae were significantly more likely to be hypertensive (p = 0.0078). Hypertensive women with abruptio placentae had the antepartum complication diabetes mellitus significantly more often than did normotensive women (p = 0.032). However, they were similar to normotensive women with regard to the frequency of positive urine drug screen and trauma. Hypertensive women were no more likely to be delivered before 32 or 37 weeks' gestation, have neonates weighing < 1500 or 2500 gm, or to be delivered by cesarean section. Abruptio placentae grades 2 and 3 occurred more often in hypertensive women (p = 0.053), as did significantly lower umbilical cord artery (p = 0.005) and venous (p = 0.003) pH values. Neonates from hypertensive women were no more likely to have low 5-minute Apgar scores or to die than those from normotensive women. CONCLUSION: Although hypertensive women experiencing abruptio placentae are more likely to have higher-grade abruptio placentae and lower umbilical cord pH values, the overall perinatal outcome was not significantly different from that of normotensive women experiencing abruptio placentae.

Abruptio Placentae↗