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PubMed2003

The effect of smoking and caffeine on the fetus and placenta in pregnancy.

The aim of this study was to determine the effects of tobacco use and consumption of caffeine in pregnancy on the fetus and placenta by measuring the body weights, head circumferences, and lengths of newborns, and also weights and diameters of placentas. In this prospective study, two main groups were chosen for the study: Group I: A total of 63 pregnant non-smokers; were separated into two subgroups according to their daily caffeine intake; less than 300 mg (Ia) (n = 44), and more than 300 mg (Ib) (n = 19). Group II: 60 pregnant smokers were also separated into two subgroups; daily caffeine intake less than 300 mg (IIa) (n = 43), and more than 300 mg (IIb) (n = 17). The newborns and placentas of both groups were examined. The body weights, lengths, and head circumferences of newborns and also weights and diameters of placentas were measured. The pregnant non-smokers consuming caffeine more than 300 mg/day had statistically significant lower weights of newborns and placentas (p < 0.05). However, there was no significant difference between groups according to the lengths, head circumferences of newborns and diameters of placentas. There were significantly lower body weights of newborns and placentas in pregnant smokers (p < 0.05). There was no difference according to the diameters of placentas, and lengths and head circumferences of newborns in either group. In conclusion, it is suggested that smoking in pregnancy should be prevented both for the health of newborns and mothers, and also caffeine including beverages like tea and coffee should be limited in pregnancy.

Anthropometry↗
PubMed2003

[Conservative treatment of placenta accreta].

OBJECTIVE: Examination of modalities and results of conservative treatment of placenta accreta. MATERIAL AND METHOD: Ten-year hospital records were reviewed, with analysis of patients who had diagnosis of placenta accreta associated with conservative treatment. RESULTS: During the study period, 21259 deliveries were registered, with an incidence of placenta accreta of 1 per 1 000 deliveries (n=23). Conservative treatment was applied in 13 patients. All of them had factors commonly associated with placenta accreta: prior cesarean sections (7/13), prior curettage or endouterine surgery (11/13), placenta praevia (11/13). Antenatal diagnosis was performed in only 64% of the cases (n=7). In our conservative strategy, placenta accreta was always left in situ, with an associated treatment in most of cases (n=10): Bilateral hypogastric artery ligation (n=7), medical treatment with methotrexate (n=5), uterine artery embolization (n=2). There was no case of maternal mortality. Conservative treatment was successful in 11 patients. It failed in 2 cases: hysterectomy was performed in one case for life-threatening hemorrhage, and in the other case for post-embolization uterine necrosis. The morbidity described was blood transfusion (n=7), endometritis (n=1), and one late hemorrhage with expelling necrotic tissue. Afterwards, 2 women became pregnant: one miscarriage and one normal term delivery. CONCLUSION: Conservative treatment of placenta accreta appears to be a efficient way to preserve fertility. Antepartum diagnosis should be improved among patients with a high risk of placenta accreta in order to optimize conservative strategy.

Abortifacient Agents, Nonsteroidal↗
PubMed2003

Histopathological evaluation of placentas in IUGR pregnancies.

Gross and microscopic examination was conducted on one hundred placentas. These included twenty five normal controls and seventy five from intrauterine growth retardation (IUGR) pregnancies. Weight of the placentas from IUGR pregnancies were less than those of normal placentas. The incidence of infarction, intervillous fibrin deposition were much higher in IUGR placentas on gross examination. Highly significant increase in the incidence of infarction, intervillous fibrin deposition, stromal fibrosis and syncytial knotting were found in IUGR placentas compared to full term normal placentas on microscopic examination. The incidence of basement membrane thickening and cytotrophoblastic hyperplasis were also higher in IUGR placentas. All the major histologic findings pointed towards reduced blood flow to the placentas resulting in the restriction of blood flow to fetus. The information obtained from their examination can be a useful adjunct in planning and management of future pregnancies.

Basement Membrane↗
PubMedDate not supplied

Abruptio placentae and its complications at Ayub Teaching Hospital Abbottabad.

BACKGROUND: Abruptio placentae remains a major cause of perinatal morbidity and mortality globally, though of most serious concern in the developing world. As most known causes of abruptio placentae are either preventable or treatable, an increased frequency of the condition remains a source of medical concern. METHODS: The present study was undertaken at the Department of Obstetrics and Gynaecology, Unit B, of the Ayub Teaching Hospital, Abbottabad, Pakistan, from July 2003 to June 2004. Patients of abruptio placentae were selected from all cases of 28 weeks or greater gestation, presenting with ante partum haemorrhage during the study period. Patients underwent a complete obstetrical clinical workup including history, general physical examination, abdominal and pelvic examination. Relevant investigations such as laboratory tests and imaging were performed. Patients were managed according to maternal and fetal condition. Any maternal and/or fetal complications were noted and recorded. All data were collected on predesigned proformas and analyzed by computer. RESULTS: A total of 53 cases of abruptio placentae were recorded out of 1194 cases (4.4%) admitted for delivery during the study period, giving a rate of 44 cases of abruptio placentae per 1000 deliveries. Induction of labour was required in 27 (50.9%) cases, while caesarean section was performed in 16 (30.2%) cases. Major complications were intra uterine fetal demise (31/53, 58.5%), fetal distress (8/22 live births, 36.4%) and post partum haemorrhage, which occurred in 10 (18.9%) cases. CONCLUSIONS: A higher than expected frequency of abruptio placentae exists in our setting and the consequences of abruptio placentae for neonatal mortality outcome are alarmingly high. The majority of patients presented with intra uterine death so that any management protocol directed at abruptio placentae or its consequences is of little help in preventing perinatal mortality.

Abruptio Placentae↗
PubMed1992

Localization of human immunodeficiency virus core antigen in term human placentas.

Evidence of human immunodeficiency virus (HIV) replication was sought in human placentas obtained at term from pregnancies complicated by maternal HIV infection. Placentas were obtained from the pregnancies of 19 HIV-seropositive women, 4 women who were seronegative, and 4 untested women with no risk factors for HIV infection. These placentas were each examined by immunoperoxidase immunocytochemistry using monoclonal anti-p24/55 antibodies. In addition, minced placental tissue from 11 of the seropositive pregnancies and the 3 seronegative pregnancies were co-cultivated with stimulated human peripheral blood mononuclear cells. The clinical status of the infants born to the HIV-seropositive women was assessed when the infants were 8 to 28 months of age. P24/55 antigen was detected in 5 of the 19 placentas of the HIV-seropositive pregnancies and in none of the 8 placentas of seronegative or low-risk pregnancies. This HIV core viral antigen was located exclusively in the cytoplasm of villous cells with morphological characteristics of macrophages. The HIV antigen-containing cells were very sparsely distributed. Staining of the trophoblast was not observed in any placental specimen. Human immunodeficiency virus was isolated in culture from 3 of the 11 placentas from seropositive pregnancies. Clinical follow-up has not revealed a relationship between infection of the infant and either p24/55 antigen identification or isolation of virus from the placenta. Virological and histological evidence of HIV replication is found in approximately one fourth of placentas obtained at term from pregnancies complicated by maternal HIV infection. Replicating virus appears localized to sparse macrophages located within the chorionic villi, but specifically not within the trophoblastic layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1991

Reduced frequency of hypertensive disorders in placenta previa.

The isthmic segment of the uterine artery's ascending branch has a freer course and wider diameter than distal parts of the vessel. Therefore, we assumed that this arterial segment would provide better blood flow and prevent hypoxia of the trophoblast. As a result, placenta previa pregnancies would be complicated by hypertensive disorders less often than are pregnancies with normally implanted placentas. To test this hypothesis, 491 placenta previa pregnancies, among a population of 106,866 pregnant women, were compared with pregnancies with normally implanted placentas. Clinically meaningful and statistically significant reductions in the rates and risks of hypertensive disorders were found in placenta previa pregnancies (P = .002, relative risk = 0.44, 95% confidence interval 0.25-0.78). The differences persisted when primiparous and multiparous women were examined separately and when preterm and term deliveries were separated. In a multivariate logistic regression analysis, patients with placenta previa had a third of the risk for hypertensive disorders compared with pregnant women with normally implanted placentas (relative risk = 0.36, 95% confidence interval 0.20-0.64), even after controlling for parity and preterm or term delivery. In the same model, primiparity and preterm delivery were each associated with a doubling of risk for hypertensive disorders, regardless of the placental implantation site. Thus, regardless of parity and preterm or term delivery, placenta previa and hypertensive disorders are inversely related.

Adult↗
PubMed1989

Effect of insulin, prostaglandin E1 and uptake inhibitors on glucose transport in the perfused guinea-pig placenta.

The effects of insulin, prostaglandin E1 (PGE1) and uptake inhibitors on unidirectional D-glucose influx at brush border (maternal) and basal (fetal) sides of the guinea-pig syncytotrophoblast were investigated in the intact, perfused guinea-pig placenta by rapid, paired-tracer dilution. Experiments were performed in either an in situ preparation artificially perfused through the umbilical vessels (intact maternal circulation) or in the fully isolated dually-perfused placenta in which both interfaces were studied simultaneously. Kinetic characterization of unidirectional D-glucose influx gave apparent Km values (mean +/- SEM) at maternal and fetal sides of 70 +/- 6 and 87 +/- 16 mM respectively; corresponding Vmax values were 53 +/- 3 and 82 +/- 6 mumol min-1g-1. At the fetal side (singly-perfused placenta) cytochalasin B (50 microM), ethylidene-D-glucose (100 mM) and PGE1 (1 microM) partially inhibited D-glucose uptake whereas cortisol (50 microM) and progesterone (100 microM) had no effect. Abolition of the sodium gradient across the fetal interface did not modulate the kinetics of influx. In the presence of 150 mu units ml-1 insulin (dually-perfused placenta), unidirectional uptake into the trophoblast and transplacental D-[3H]glucose transfer were unaltered. In contrast, prostaglandin E1 (1 microM) markedly reduced the Km and Vmax for D-glucose at both interfaces and the inhibitory effect was reflected in a reduction in specific transplacental D-glucose transfer. Further experiments showed that the isolated placenta releases prostaglandins (PGE; PGF2 alpha) into both circulations. Bilateral insulin perfusion did not affect either lactate release by the placenta or rapid metabolism of D-[14C]glucose to [3H]lactate (usually less than 10% effluent [14C]lactate in 5 min). An asymmetric degradation of exogenous insulin was observed in the dually-perfused placenta: uterine venous samples contained 24 +/- 7 microunits ml-1 immunoreactive insulin when compared to the arterial concentration (151 +/- 3 microU ml-1 perfusate) while no change was measureable in the fetal circulation within the same time period (152 +/- 5 microU ml-1). This asymmetry was confirmed in experiments employing [125I]insulin. These results demonstrate that glucose transport in the intact guinea-pig placenta occurs by a sodium-independent, cytochalasin B-inhibitable system which is insulin-insensitive. Prostaglandin E1 appeared to be a potent transport inhibitor which suggests that prostaglandins may be involved in the 'down' regulation of placental glucose transport in vivo.

Alprostadil↗
PubMed1988

Effects of histamine on vascular resistance and protein permeability in the isolated dually perfused guinea-pig placenta.

The possibility that histamine can affect both the vascular resistance and permeability of the isolated dually perfused guinea-pig placenta has been investigated. Change from control to histamine (2.7 x 10(-4)M) perfusion of the fetal circulation elicited a significant (P less than 0.01, paired 't' test) maximum increase of 1.17 +/- 0.14 (SEM) kPa in fetal perfusion pressure 3 min later, representing a 33% rise. This vasoconstriction was completely blocked by the H1 antagonist diphenhydramine (10(-4)M) but not by the H2 receptor antagonist cimetidine (10(-4)M). In the same experiments the clearance (calculated as the ratio of fetal to maternal perfusate concentration times fetal flow-rate) of a macromolecular tracer, anionic horseradish peroxidase from the maternal to fetal circulation was significantly increased (P less than 0.05, paired 't' test) when steady state (15-20 min of perfusion) values were compared, from 5.9 +/- 1.7 (SEM) microliter min-1 placenta-1 to 12.9 +/- 3.5 (SEM) microliter min-1 placenta-1 (n = 20) for control and histamine respectively. By contrast the steady state clearance (calculated as before) of a smaller hydrophilic tracer, 51Cr-EDTA, was not significantly affected, being 587 +/- 59 (SEM) microliter min-1 placenta-1 in control and 587 +/- 55 (SEM) microliter min-1 placenta-1 (n = 20) with histamine perfusion. When histamine was perfused simultaneously with an H1 or H2 antagonist there was no change in anionic horseradish peroxidase clearance. Electron microscopy of placentas perfused with histamine failed to reveal any obvious alteration in morphology or anionic horseradish peroxidase localisation as compared to placenta perfused without histamine. This study thus demonstrates that histamine may cause changes in the macromolecular permeability of the placenta as well as vasoconstriction of the placental vasculature.

Animals↗
PubMed1987

[Immunohistochemical and biochemical investigations on glutathione S-transferases in the human placenta].

GST-pi can be purified as a major molecular form of glutathione S-transferase (GST) in human placenta. In this paper, the localization of GST-pi as well as of neutral and basic GSTs in the first, second and third trimester placental tissues (10, 3 and 14 samples, respectively) was investigated immunohistochemically using antibodies to acidic GST-pi from the placenta, neutral GST-mu and basic GST-I from the liver. Total GST activity was assayed using 1-chloro-2,4-dinitrobenzene as a substrate, and the relative activity and content of GST-pi were determined by activity inhibition test and single radial immunodiffusion, respectively, on 4 first and 5 third trimester placental tissues. The results obtained were as follows. In early placenta, cytotrophoblasts were strongly stained by anti-GST-pi antibody, while in third placenta mainly syncytiotrophoblasts were stained. GST-mu was stained only in syncytiotrophoblast in early placenta, while basic GST-I was weakly stained in the various cells in early to term placenta. Total GST activity in early and term placentas was 5.8 +/- 2.0 units/g of tissue (mean +/- S.D.) and 14.8 +/- 3.4 units/g, respectively. GST-pi relative activities were 90 +/- 4% and 85 +/- 6%, and GST-pi content was 41 +/- 31 micrograms/g and 106 +/- 29 micrograms/g, respectively. These results indicate that GST-pi is a major form of GST and localized mainly in trophoblasts at any developmental stage of the placenta, and it increases with development.

Cell Cycle↗
PubMed1984

Human placenta aldose reductase. Forms sensitive and insensitive to inhibition by alrestatin.

The inhibition of aldose reductase from a human source by alrestatin was studied. The enzyme from placenta was purified to apparent homogeneity by (NH4)2SO4 precipitation, DEAE-cellulose chromatography, electrofocusing, and affinity chromatography. This enzyme from human or rat placenta at the (NH4)2SO4 state of purification was relatively insensitive to alrestatin (IC50 greater than 50 microM). On purification by electrofocusing, however, human or rat placenta aldose reductase exhibited a marked increase in its sensitivity to alrestatin (IC50 = 1.0 microM). In contrast to human or rat placenta aldose reductase, rat lens aldose reductase was equally sensitive to alrestatin at the corresponding stages of purification (IC50 = 1.0 microM). Experiments in which the sensitive and insensitive forms of placenta aldose reductase were mixed revealed that the difference in susceptibility to alrestatin could not be attributed to nonspecific binding of alrestatin by proteins present in the (NH4)2SO4 fraction. A heat-inactivated (NH4)2SO4 fraction of human placenta aldose reductase added to the sensitive placenta enzyme from human or rats caused a time-dependent conversion to the insensitive form of aldose reductase. This suggested that a heat-stable dissociable factor, associated with placenta aldose reductase at the crude stage, may be responsible for the insensitivity to alrestatin. This insensitivity could be of pharmacological significance if it is relevant in vivo and it exists in tissues where aldose reductase plays a physiological role.

Aldehyde Reductase↗
PubMed1981

[Study on the metabolism of prostaglandin F2 alpha in human placenta (author's transl)].

The activity of 15-hydroxy prostaglandin dehydrogenase (15 OH-PGDH) was studied in the human placenta by the biochemical determination and enzyme histochemical technique. The placentae of 6-40 weeks of gestation were obtained from artificial abortion, spontaneous abortion and normal delivery. 1) The capability of prostaglandin metabolism in the placenta increased according to gestational age. 2) The relative potency of 15 OH-PGDH activity among different tissues was placenta villi greater than chorion greater than decidua greater than amnion. The enzyme histochemical technique has disclosed the same results. 3) The conversion rate of PGF2 alpha to 15-keto PGF 2 alpha was dominant in the maternal side rather than fetal blood vessel system in the perfusion experiment of placenta. 4) The strong activity of 15 OH-PGDH was mainly localized in the syncytiotrophoblasts of placenta villi. 5) The activity of 15 OH-PGDH decreased in the placenta of abortion. The decrease of this enzyme activity was not detected in the toxemia of pregnancy. It has been postulated that endogenous and exogenous prostaglandin, which possesses strong and multiple biological activity, increases in the pregnancy. The present results suggest that the prostaglandin metabolic system in the placenta has the important role in the continuity of pregnancy.

Chorionic Villi↗
PubMed1980

[Use of high-speed ultrasonography for differential diagnosis of gestational haemorrhage, following formation of placenta (author's transl)].

The "Vidoson 635-S" high-speed ultrasonographic unit was used by the authors to examine 465 women pregnant in the second and third trimenons for the occurrence of bleeding. The following findings were obtained: NAD (no abnormality discovered), Placenta praevia totalis, Placenta praevia partialis lateralis, Placenta praevia partialis marginalis, deep adherence of placenta, early detachment of placenta, and uterus rupture. - Placental displacement was observed by repeated checking in 57 of 196 placentas with pathological findings. Placental prolapse observed between the twelfth and 20th weeks of pregnancy was defined as "early" Placenta praevia, and the birth canal was left in about 50 per cent of those cases. The authors' view about such phenomenon was that while the point of placental adherence was unchanged, some change was undergone by the uterus wall of which that part changed position to which the placenta adhered, the latter dislocation being caused by enlargement of the upper third of the passive uterus region and its part in the formation of the uterus cavity.

Diagnosis, Differential↗
PubMed1994

Neoplastic hormone-producing cells of the placenta produce and secrete parathyroid hormone-related protein. Studies by immunohistology, immunoassay, and polymerase chain reaction.

BACKGROUND: Parathyroid hormone-related protein (PTHrP) was originally discovered as a product of tumors associated with hypercalcemia. Subsequent studies have demonstrated the widespread production of PTHrP in both fetal and adult tissues, among them the placenta, where it has been identified in amniotic epithelial cells and trophoblasts. However, studies of PTHrP production by the neoplastic placenta have not been reported. EXPERIMENTAL DESIGN: We have studied placental cells and tissues for PTHrP by immunohistology, immunoassay, and the polymerase chain reaction. We studied normal placenta, placenta neoplasia, and placental cell lines grown in culture. RESULTS: Our studies in abnormal placenta demonstrate that PTHrP is produced by chorioangioma, choriocarcinomas, and hydatidiform moles, indicating that PTHrP may be a marker for neoplasia of the placenta. Our studies in normal placenta demonstrate that PTHrP is produced by several placental cell types, including, syncytiotrophoblast, intermediate trophoblasts, cytotrophoblasts, and amniotic epithelium, suggesting an important role for this protein in several aspects of placental function. Cell lines derived from trophoblasts and amniotic epithelium also produced PTHrP and secreted it into culture medium. Polymerase chain reaction with PTHrP coding sequence primers demonstrated the appropriate polymerase chain reaction product in these placental cells. CONCLUSIONS: The production of PTHrP by several normal and abnormal placental cell types is evidence for an important function for PTHrP in normal and neoplastic placenta.

Cell Line↗
PubMedDate not supplied

Antioxidant activities and mRNA expression of superoxide dismutase, catalase, and glutathione peroxidase in normal and preeclamptic placentas.

OBJECTIVE: Placental production of lipid peroxides is abnormally increased in preeclampsia. The reason for this is not known, but if placental antioxidant enzymes were deficient, lipid peroxides would increase unchecked. In this study, we measured 1) enzyme activities of superoxide dismutase (CuZn-SOD), catalase, and glutathione peroxidase (GSH-Px) and tissue levels of vitamin E, and 2) mRNA expression of CuZn-SOD, catalase, and GSH-Px in normal and preeclamptic placentas. METHODS: Placental tissues were obtained from normal (n = 16) preeclamptic (n = 12) pregnancies immediately after delivery. Tissue pieces were frozen in liquid nitrogen and stored at -80C until assayed. The enzyme activities of CuZn-SOD, catalase, and GSH-Px and the levels of vitamin E were determined by spectrophotometric assays. Messenger RNA expression of CuZn-SOD, catalase, and GSH-Px was determined by Northern blot analysis. RESULTS: The activities of CuZn-SOD and GSH-Px and the tissue levels of vitamin E were significantly lower in preeclamptic placentas than in normal placentas (CuZn-SOD: 1.13 +/- 0.49 versus 3.71 +/- 0.71 U/mg protein, P < .01; GSH-Px: 0.18 +/- 0.01 versus 0.26 +/- 0.02 U/mg, P < .01; vitamin E: 0.08 +/- 0.01 versus 0.18 +/- 0.01 microgram/mg, mean +/- standard error, P < .001), whereas the activity of catalase was significantly higher (93 +/- 3 versus 83 +/- 2 U/mg, P < .05). Relative mRNA expression of CuZn-SOD and GSH-Px was significantly lower in preeclamptic than normal placentas (P < 0.05), but there was no significant difference for catalase (P > .4). CONCLUSIONS: 1) Activities of CuZn-SOD and GSH-Px and the tissue levels of vitamin E are significantly lower in preeclamptic than in normal placentas. 2) Activity of catalase is significantly higher in preeclamptic than in normal placentas. 3) Messenger RNA expression for CuZn-SOD and GSH-Px is lower in preeclamptic placentas. We speculate that decreased antioxidant activity may result in increased lipid peroxide levels in preeclamptic placentas.

Antioxidants↗
PubMedDate not supplied

Relationship between human immunodeficiency virus-1 RNA identification in placenta and perinatal transmission.

OBJECTIVES: The objectives of this study were to identify human immunodeficiency virus (HIV)-associated nucleic acids in placenta with 35S RNA in situ hybridization and to correlate the presence of virus with perinatal HIV transmission. STUDY DESIGN: Blood from nine mother-infant pairs was collected for CD4+ lymphocyte count and p24 antigen analysis. Placental specimens were obtained for in situ hybridization, viral culture, and hematoxylin-eosin histologic analysis. Neonatal infection was diagnosed by p24 antigen analysis, polymerase chain reaction, and viral culture. Pediatric follow-up was obtained by personal communication and review of chart records. RESULTS: Three of 10 placentas from nine HIV-positive pregnant women (one set of twins) were found to contain evidence of HIV infection by RNA in situ hybridization. Maternal age, gravidity, parity, previous number of terminations, duration HIV-seropositive, maternal CD4+ at delivery, and neonatal cord CD4+ count were similar in those whose placentas contained virus versus those in whom virus was not identified. The incidence of histologic changes was similar in the HIV-positive and negative placentas from seropositive subjects and was similar to the incidence of histologic changes in placentas from known seronegative subjects. Placental culture failed to demonstrate the presence of virus in vitro. Of the three placentas that had positive in situ hybridization, two infants became HIV-positive. CONCLUSIONS: 35S RNA in situ hybridization identified the presence of nucleic acids in syncytiotrophoblasts from formalin-fixed, paraffin-embedded placentas. This technique is a useful tool to screen placentas at birth for HIV-RNA to judge the likelihood of perinatal HIV transmission.

Adult↗
PubMed1990

Pathologic analysis of preterm delivery placentas.

198 preterm delivery placentas of 28 weeks to less than 37 weeks pregnancy were analyzed. Gross examination revealed that the differences of placenta previa and low implantation (2.91%), bipartate placenta and rupture of marginal sinus (0.97% respectively), large placenta (2.91%), short cord (4.85%), velamentous insertion of cord (3.88%), etc in comparison with those of term delivery placentas were statistically significant. Microscopic examination of 165 placentas showed that in 19 cases (11.52%) of infection of membranes and umbilical vessels, 11 were due to premature rupture of membranes or cervical interventions and 8 to preterm delivery. Among 72 cases of PIH, 65 (90.28%) had arteriopathy of decidua capsularis. 18 cases (25%) which had not been diagnosed clinically as PIH were found to be neglected after discovery of arteriopathy of decidua capsularis by pathologic examination. Placental examinations showed that preterm delivery may be attributable to the factors of placenta, amniotic fluid and umbilicus. 20 cases (27.78% of total PIH) of premature rupture of membranes were complicated by PIH. Whether the cases of decidual arteropathy are liable to have rupture of membranes awaits further investigation.

Female↗
PubMed1988

Dose-dependent enhancement of morphine-induced analgesia by ingestion of amniotic fluid and placenta.

Ingestion of amniotic fluid and placenta by rats has been shown to enhance opioid-mediated analgesia. The present studies were designed to examine the effect of several doses and volumes of placenta and amniotic fluid on tail-flick latency in rats treated with 3 mg/kg morphine. The optimal dose of amniotic fluid was found to be 0.25 ml, although 0.50 and 1.0 ml also produced significant enhancement. Doses of 0.125 and 2 ml of amniotic fluid were ineffective, as was a dose of 0.25 ml diluted to 2 ml with saline. The optimal dose of placenta was found to be 1 placenta, although the resulting enhancement was not significantly greater than that produced by 025, 0.50, 2.0 or 4.0 placentas. Doses smaller than 0.25 placenta or larger than 4.0 placentas were ineffective. The most effective doses of amniotic fluid and placenta correspond to the amounts delivered with each pup during parturition.

Amniotic Fluid↗
PubMed2005

PAF levels and PAF-AH activities in placentas from normal and preeclamptic pregnancies.

OBJECTIVE: The aim of this study was to determine: (1) platelet-activating factor (PAF) levels and PAF-acetylhydrolase (PAF-AH) activities in normal and preeclamptic placentas; (2) lipid peroxide production by placental tissues stimulated with PAF. METHODS: Placentas were obtained immediately after delivery from normal and preeclamptic pregnancies. Tissue pieces were snap frozen in liquid nitrogen and stored at -70 degrees C. One gram of tissue from each placenta was used for PAF extraction and for total RNA isolation. PAF was measured by PAF [3H] scintillation proximity assay (SPA) system. Trophoblast PAF-AH activity was determined by enzyme-linked immunosorbent assay (ELISA). mRNA expression for PAF receptor was assessed by RNase protection assay (RPA). Normal placental explants were incubated with PAF at concentrations of 1 and 10 microg/ml for 48 h. Lipid peroxide productions of 8-isoprostane and malondialdehyde (MDA) were measured by ELISA and thiobarbituric acid reaction, respectively. Data were presented as mean+/-SE and analyzed by nonparametric Mann-Whitney U test and ANOVA. A p level less than 0.05 was considered statistically significant. RESULTS: (1) The mean tissue level for PAF was elevated, but not statistically different, in preeclamptic (n=7) than in normal (n=8) placentas, 6.45+/-1.05 versus 4.47+/-0.60 ng/g, p=0.42. (2) PAF-AH activity was higher in trophoblasts from preeclamptic (n=7) placentas than that in trophoblasts from normal (n=8) placentas, 0.69+/-0.16 versus 0.38+/-0.03 micromol/min/microg protein, p<0.05. (3) The relative mRNA expression for PAF receptor was not different between normal (0.70+/-0.08) and preeclamptic (0.76+/-0.13) placental tissues, p=0.60. (4) Productions of 8-isoprostane and MDA were not increased in tissues with PAF in culture, 8-isoprostane: 0.37+/-0.09 ng/mg (control) versus 0.32+/-0.09 ng/mg (1 microg/ml) and 0.37+/-0.07 ng/mg (10 microg/ml), p>0.5; MDA: 0.62+/-0.05 nmol/mg (control) versus 0.68+/-0.04 nmol/mg (1 microg/ml) and 0.69+/-0.03 nmol/mg (10 microg/ml), p>0.5. CONCLUSIONS: Increased PAF-AH activity in trophoblasts may be a compensatory effect to control PAF level in the preeclamptic placenta. The co-existence of PAF-AH and PAF receptor in trophoblasts suggests an autocrine regulation of PAF in these cells to limit PAF and its metabolites within the placenta.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗