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At least 19 recordsLinked to original sources

PubMed1977

[New aspects in diagnosis and therapy of placental insufficiency. Placental perfusion measurements; placental perfusion test (PPT) and betamimetic long term treatment (clinical and experimental data (authors transl)].

The rate of utero-placental blood flow depends on functional components (perfusion pressure and flow resistance within the area of the vascular bed of the placenta), as well as on morphological factors (regressive changes in the placenta). Different primary maternal conditions and diseases may lower the rate of placental flow, leading to placental insufficiency; the highest percentage, by far, of placental dysfunction is found in patients suffering from gestosis. Hypocirculation initially present in cases of EPH gestosis and caused by arteriolar spasms triggers off a vicious circle involving placental infarction and severe reduction in the utero-placental perfusion rate. This in turn leads to fetal hypotrophy, a high rate of premature births and perinatal mortality. Verification of HPL, HCG, alpha-Fetoprotein or E3 in maternal serum and amniotic fluid or urine greatly improved the recording of partial placental functions. Along with ultrasonic biometry, cardiotocography and amnioscopy, these hormonal parameters allow only indirect assessment of the placental function. On the other hand, measurements of the utero-placental flow offers a direct approach. In order to evaluate the placental flow measurements it is imperative to obtain a curve indicating the course over the last third of the pregnancy-in addition to establishing a general normal range. In case of placental insufficiency, it is necessary to determine whether this is due to functional disorders alone, or to more extenisve morphological changes. A placental perfusion test (PPT) was developed in order to make this distinction. Beta2-mimetic treatment is indicated if functional factors predominate, whereby it appears essential to obtain the requisite experimental data for precise quantification of beta-mimetic action.

Adrenergic beta-Agonists↗

PubMed1991

[Placental maturity at term and functional placental performance: CTG changes in relation to histologic detection of placental maturation reserves].

Cardiotocography (CTG) is to be considered today's most sensitive monitoring tool for the functional surveillance of placental performance during parturition. 351 cardiotocographically monitored singleton pregnancies were used as patient material for fine tissue examination of the state of maturity of the villi of the relevant placentas. In histological assessment, placental diagnoses are allocated to defined CTG changes; in particular, however, the identification of reserves, capable of maturing (immature intermediate villi in the centres of the placental subdivisions or placentones), is subject to separate scrutiny. The following results emerge clearly: terminal placentas without maturing potentials, prematurely matured placentas and placentas with deficiency of terminal villi, as well as the absence of immature intermediate villi in the centers of the placentones, are connected with a suspected prepathological or pathological CTG assessment. The histological groups have the lowest incidence of the normal oscillatory type and normal oscillatory frequency and have the highest proportion of abnormal CTG assessments according to the Hammacher score. The absence of the identification of potential maturing reserves (immature intermediate villi) is associated with the highest incidence of Caesarean sections (29.8%). These results show, that the physiological maturing potentials (immature intermediate villi) which can be identified up to term are a histological indication towards regular placental performance, even in labour.

Cardiotocography↗

PubMed1975

[Serum placental lactogen in late pregnancy and its relation to placental villous surface and to placental maturation (author's transl)].

The placentas of ninety-six pregnancies supervised by measurements of human placental lactogen (HPL) were examined. The histometrically determined placental villous surface and the degree of maturation of the villous tissue were compared to HPL-values in late pregnancy and to the weight of the newborn. The production of HPL is dependent on the extent of the syncytiotrophoblast surface area and, in addition, is modulated by the grade of differentiation of the chorionic epithelium. Placental villi with abnormalities of maturation apparently synthesize more HPL than villi of normal maturation.

Birth Weight↗

PubMed1990

Placental site trophoblastic tumor: with features between an exaggerated placental site reaction and a placental site trophoblastic tumor.

Chorionic villi, whose presence in cases of trophoblastic disease is normally used to exclude both a choriocarcinoma and placental site trophoblastic tumor (PSTT), were present in the initial uterine curettage specimen of a trophoblastic tumor. The lesion shared morphologic features of both an exaggerated placental site reaction and a PSTT. There was infiltration of the posterior wall of the uterus by small clusters and isolated cells which had a prominent affinity for vessels and resembled a usual placental bed reaction. There was, however, deep involvement of myometrium with extension to the cervix, and the condition persisted for 5 months after uterine evacuation. Because different treatment is entailed, identification of this lesion as a tumor of nonvillous trophoblast is also of great importance in a region where the more usual forms of trophoblastic disease represent a declining but not infrequent event. When products of gestation are examined, the possibility of a PSTT should be considered and the clinician alerted if there is a suggestion of excessive intermediate trophoblastic activity, regardless of the presence of chorionic villi. While this may result in the unnecessary followup of some cases, it would permit, with the aid of serial beta-hCG and HPL levels, the earlier detection of PSTTs.

Adult↗

PubMed1987

[The changes in EPH gestosis placental amino acid transport activity (using human placental microvillous membrane vesicles)].

To elucidate the change in EPH gestosis placental amino acid transport activity, we investigated the uptake of L-alanine into microvillous membrane vesicles prepared from EPH gestosis placenta and from normal placenta by using a rapid filtration technique. 1. Alkaline phosphatase (ALP) was the marker enzyme of microvillous membrane vesicles (MMV). The ALP activity of mild EPH gestosis placental MMV didn't differ from that of normal placental MMV. On the other hand, the ALP activity of severe EPH gestosis placental MMV decreased compared to that of normal placental MMV. 2. The uptake of L-alanine into human placental MMV was dependent on the Na+ electrochemical gradient, so the transport across human placental MMV was a secondarily active one. The L-alanine transport activity of mild EPH gestosis placental MMV didn't differ from that of normal placental MMV. On the other hand, the L-alanine transport activity of severe EPH gestosis placental MMV decreased prominently compared to that of normal placental MMV.

Alanine↗

PubMed1991

Placental toxicology: tobacco smoke, abused drugs, multiple chemical interactions, and placental function.

There are increasing numbers of reports on the tobacco smoking and ingestion of abused drugs (e.g. morphine, cocaine) by pregnant women and the effects of the substances on the developing fetus and newborn infant. The passage of drugs and chemicals from the mother to the fetus is influenced by the placental transport and metabolism of the substances. Further, these drugs and chemicals affect the nutrient transport systems in the placenta. The three major drugs of abuse-nicotine, morphine and cocaine-depress both active amino-acid uptake by human placental villi and transplacental amino-acid transport by reason of the drugs' influence on placental cholinergic and opiate systems. Part of this depression (10-16%) is not reversible. Nicotine blocks the cholinergic receptor and thus blocks acetylcholine (ACh)-facilitated amino-acid transport. Morphine stimulates opiate kappa receptors and depresses ACh release. Cocaine blocks Ca2+ influx and thus blocks ACh release. ACh causes dilation of blood vessels and maintains placental blood flow by the activation of endothelial muscarinic receptors. By interfering with ACh release and placental blood flow, the three drugs of abuse may depress the diffusion of amino acids and other nutrients from the trophoblast into the placental circulation. Three regulatory systems are delineated for amino-acid uptake by the placenta: placental ACh, phospholipid N-methyltransferase, and the gammaglutamyl cycle. These systems operate in concert with one another and are dependent on cellular formation of adenosine 5'-triphosphate (ATP). Placental hypoxia induced by carbon monoxide and other tobacco gases depresses the energy-dependent processes and thus the ATP levels of placental cells. Maternal tobacco smoking and drug abuse cause placental insufficiencies for amino-acid transport, which may partially explain the fetal intrauterine growth retardation caused by these substances. Part of the amino-acid deficits may be compensated for by the induction of new amino-acid transport systems. Specific receptors or drug-binding proteins for the three drugs of abuse are present in the placenta. A DNA adduct selective for maternal smoking has been demonstrated in the placenta. DNA adducts selective for cocaine, morphine and other environmental chemicals have yet to be demonstrated ins the placenta.

Amino Acids↗

PubMed1987

Effect of restriction of placental growth on fetal and utero-placental metabolism.

The effect of restriction of placental growth on the supply of glucose to the gravid uterus and fetus and on fetal and utero-placental metabolism of glucose and lactate was examined in this study. Endometrial caruncles were removed from 13 sheep (caruncle sheep) prior to mating, which restricted placental growth in the subsequent pregnancy. Half the fetuses of caruncle sheep were small or growth retarded, with the remainder normal in size. After insertion of vascular catheters at 110 days gestation, the caruncle sheep, together with 16 control sheep, were studied between 121 and 130 days of gestation. Glucose delivery to and consumption by the gravid uterus and its contents, both as a total and per kg of tissue mass, was significantly lower in caruncle ewes with small fetuses, although glucose extraction was similar to that in controls. Utero-placental glucose consumption was significantly lower in caruncle ewes carrying small fetuses compared to that in control ewes, both as a total and per kg of placenta. Small caruncle fetuses were hypoxaemic and hypoglycaemic and the lactate concentration in the common umbilical vein was significantly higher than in control sheep. Glucose delivery to and consumption by the fetus was significantly lower in normal-sized and in small caruncle fetuses compared to controls. Fetal glucose consumption per kg of fetus was similar in control and caruncle sheep. Fetal glucose extraction increased as fetal weight decreased. Utero-placental production of lactate was similar in control and caruncle ewes. However, uterine output of lactate decreased as placental weight fell. Utero-placental production of lactate per kg of placenta was significantly higher in caruncle ewes compared to controls and increased as oxygen content in blood from the fetal femoral artery decreased. Fetal lactate consumption per kg of fetus increased as the concentration of lactate in blood from the common umbilical vein increased. It is concluded that intrauterine growth retardation due to restriction of placental growth is associated with a reduced supply of glucose to both the pregnant uterus and fetus and a redistribution of glucose therein to the fetus, both directly as glucose and indirectly as lactate. This reflects the disproportionate maintenance of fetal weight relative to that of the placenta, reduced utero-placental consumption of glucose per kg of placenta, conversion of a greater proportion of that glucose or other substrate(s) to lactate by the placenta and an increase in the fraction of the lactate produced by utero-placental tissues that is secreted into the fetal circulation.

Animals↗

PubMed1987

Effects of continuous intravenous infusion of an ovine placental extract enriched in placental lactogen on plasma hormones, metabolites and metabolite biokinetics in non-pregnant sheep.

Continuous intravenous infusions of saline or of a placental extract containing ovine placental lactogen were given to three non-pregnant, non-lactating ewes over periods of 36 h, 1 week apart. During saline infusion no placental lactogen was detected in jugular vein plasma. but infusion of the placental extract raised the placental lactogen concentration from undetectable to 40-50 micrograms/l, similar to concentrations in ewes with one fetus on day 90 of pregnancy. By comparison with the saline control period, infusion of the placental extract consistently increased both plasma concentrations and irreversible loss of nonesterified fatty acids. Plasma concentrations of glucose and urea, but not irreversible loss of these metabolites, were consistently increased. Although the placental extract was not subjected to extensive purification, it was enriched in placental lactogen and contained no detectable contamination with insulin, prolactin or growth hormone. The results are suggestive of a role for placental lactogen in modifying metabolism and acting during pregnancy to provide nutrients for fetal metabolism.

Animals↗

PubMed1989

[The correlation of reduced amniotic fluid volume, placental maturity and morphologic placental changes in placental insufficiency].

A reduced quantity of amniotic fluid is diagnosed semiquantitatively in 41 pregnant women in the 38th to 40th week of gestation. In 21 cases, the birth of a mature hypotrophic child below the 10th weight percentile is registered. Sonographically, the placentas of the mature eutrophic children significantly more frequently show a grade III maturity and the placentas of the mature hypotrophic children a grade II maturity. In contrast to the values found in the placentas of eutrophic children and in the placentas with grade III maturity, a significantly decreased villous vascularization is determined in the placentas of hypotrophic children and in placentas with grade II maturity. The area of attachment of the placenta is 301 cm2 for the eutrophic children and 222 cm2 for the hypotrophic children. All findings are discussed and compared with the relevant data of the pertinent literature.

Amniotic Fluid↗

PubMed1987

Bovine placental prostaglandin synthesis in vitro as it relates to placental separation.

Bovine placentomes were collected during late gestation, prepartum and immediately postpartum. Postpartum tissues were collected prior to fetal membrane separation. Maternal and fetal placentomal components each were examined for their ability to synthesize prostaglandins (PG's) from arachidonic acid (AA) and metabolize PGF2 alpha and PGE2 in vitro. Maternal placental PG synthesis was lower (P less than .05) than that for fetal placental tissue and was primarily PGF's. Fetal placental PG synthesis increased (P less than .05) prepartum and was primarily PGE's. Fetal placental PGE production predominated (P less than .05) postpartum if the fetal membranes were retained, while PGF production predominated (P less than .05) if the membranes were released. Maternal and fetal placental tissues were unable to convert PGE2 to PGF2 alpha (P greater than .05). Postpartum fetal placental tissue was able to convert PGF2 alpha to PGE2 (P less than .05) if the fetal membranes were retained but not if the membranes were released (P greater than .05). These results indicate that fetal placental synthesis of PGF's may be related to placental membrane separation. The shift in fetal placental PG production from PGE's to PGF's may be due to a cessation of the ability of released fetal tissue to convert PGF2 alpha to PGE2.

Animals↗

PubMed1985

In vitro degradation of oxytocin by pregnancy serum, placental subcellular fractions and purified placental aminopeptidases.

The degradation of oxytocin (formula; see text) by human placental particulate and soluble fractions, pregnant and non-pregnant sera, and purified enzymes such as microsomal placental leucine aminopeptidase (P-LAP), retroplacental serum P-LAP and placental post-proline endopeptidase, was studied by measuring liberated amino acids with a high performance liquid chromatograph (HPLC). While the placental particulate fraction degraded oxytocin almost completely into single amino acid and amide, the placental soluble fraction did not liberate any amino acid and amide. Purified retroplacental P-LAP liberated Tyr2, Ile3, Gln4 and Asn5 from the cyclic structure of oxytocin actively. Pregnancy serum containing the retroplacental P-LAP liberated also these amino acids and amides. Purified microsomal P-LAP liberated Leu8 in addition to these amino acids and amides. Although purified placental post-proline endopeptidase or porcine kidney leucine aminopeptidase (LAP) could not liberate any amino acid and amide from oxytocin, the combination of the post-proline endopeptidase with porcine kidney LAP or with placental microsomal P-LAP actively liberated all amino acids and amides detectable by HPLC. When the ratio of amino acid liberation velocity to LAP activity measured with leu-p-nitroanilide was calculated, the ratios for cyclic amino acids such as Tyr2 and Ile3 were high with the placental particulate fraction, the mixture of post-proline endopeptidase and microsomal P-LAP, retroplacental P-LAP, and pregnancy serum. The ratio for Leu8 was high with the placental particulate fraction and the mixture of post-proline endopeptidase and microsomal P-LAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1987

Restriction of placental size in sheep enhances efficiency of placental transfer of antipyrine, 3-O-methyl-D-glucose but not of urea.

When placental growth is restricted, fetal growth is reduced but the fetal to placental weight ratio increases, suggesting that the efficiency of placental transfer may have increased. Therefore, placental transfer of antipyrine, 3-O-methyl-D-glucose and urea was measured in control pregnant sheep and in sheep with restricted placental growth (pre-pregnancy excision of endometrial caruncles). Clearance of each decreased with placental weight but clearance of antipyrine and of 3-O-methyl-D-glucose per kg of placenta increased as placental weight decreased. The small placenta exhibited increased efficiency of flow-determined transfer of antipyrine and of facilitated-diffusion transfer of glucose but not of passive transfer of the hydrophilic substance, urea. These compensatory changes should help to maintain oxygen and glucose to the fetus when the growth of the placenta has been limited by reduction of the number of placental attachment sites.

3-O-Methylglucose↗

PubMed1991

Effects of nifedipine on normotensive rat placental blood flow, placental weight and fetal weight.

Recently, nifedipine (Ca antagonist) has been used for the treatment of preeclampsia. In this study, we investigated the effects of nifedipine on the normotensive Wistar Kyoto rat's placental blood flow, fetal weight and placental weight. We measured the rat's placental blood flow using clearance of hydrogen gas generated by electrolysis. The placental blood flow, placental and fetal weights of nifedipine-treated rats (5, 10 and 25 mg/kg) were significantly (p less than 0.05) reduced compared with normal pregnant rats. These data suggest that nifedipine might have some reducing effects on placental blood flow, fetal weight and placental weight.

Animals↗

PubMed1990

Transplantable rat choriocarcinoma cells express placental lactogen: identification of placental lactogen-I immunoreactive protein and messenger ribonucleic acid.

The purpose of this investigation was to evaluate the abilities of a transplantable rat choriocarcinoma (Rcho) to produce placental PRLs. The Rcho tumor was analyzed biochemically and histologically for the expression of placental PRLs. Expression of placental PRL mRNAs was determined by Northern blot and in situ hybridization analyses. Expression of placental PRL proteins was determined by Western blot and immunocytochemical analyses. Histologically, Rcho tumors were characterized by the appearance of giant cell surrounding hemorrhagic regions. Female rats bearing the Rcho tumor beneath their kidney capsule showed extensive mammary gland development. The Rcho tumors expressed placental lactogen-I (PL-I) mRNA and protein, but there was no evidence of placental lactogen-II (PL-II), PRL-like protein-A (PLP-A), or PRL-like protein-B (PLP-B). Rcho PL-I mRNA and proteins migrated as a 1-kilobase species and a 36- to 40-kDa species similar to those expressed by normal rat trophoblast tissues. The cell type responsible for Rcho PL-I production was the giant cell, similar to that observed in normal rat trophoblast tissues. In summary, we have demonstrated the production of PL-I by a transplantable rat choriocarcinoma (Rcho). The Rcho tumor resembles rat trophoblast tissue at early postimplantation stages (days 6-10 of gestation) and may be a useful tool for studying placental PRL expression during trophoblast differentiation.

Animals↗

PubMed1977

Measurement of placental blood flow in the pig and its relation to placental and fetal weight.

In 12 pregnant sows (Sus scrofa domestica), containing 144 live fetuses, placental blood flow was measured by the indicator fractionation technique using radioactive microspheres. In 8 of these litters, which contained 96 live fetuses, placental blood flow as obtained in absolute units. Significant positive correlations were observed between placental blood flow and placental weight, between placental blood flow and fetal weight, and between placental weight and fetal weight. It is clear that the runt, by comparison with his littermates, has a low birthweight in association with a small placenta and a low placental blood flow.

Animals↗

PubMed1991

Effects of ketanserin--a serotonin receptor antagonist--on placental blood flow, placental weight and fetal weight of spontaneously hypertensive rats and normal Wistar Kyoto rats.

Recently, ketanserin (serotonin receptor antagonist) has been reported to be beneficial in the treatment of preeclampsia. In this study, we investigated the effects of ketanserin on the placental blood flow, fetal weight and placental weight in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). We measured the rats' placental blood flow by monitoring the clearance of hydrogen gas generated by electrolysis. In ketanserin (12, 24, 48 mg/kg)-treated SHR, systolic blood pressure was significantly decreased. The placental blood flow was significantly (p less than 0.05) reduced compared to that before treatment in WKY and SHR. The fetal weight decreased dose dependently in WKY, while in SHR it did not decrease significantly. The placental weight of ketanserin-treated rats decreased compared to that before treatment. These data suggest that ketanserin might have some reducing effects on placental blood flow, fetal weight and placental weight proportional to the dose.

Animals↗

PubMed1985

In vitro degradation of angiotensin II (A-II) by human placental subcellular fractions, pregnancy sera and purified placental aminopeptidases.

The degradation of angiotensin II (Asp1-Arg2-Val3-Tyr4-Ile5-His6-Pro7-Phe8: A-II) by human placental particulate and soluble fractions, pregnant and non-pregnant sera, and highly purified placental enzymes such as placental leucine aminopeptidase P-LAP (microsomal), retroplacental serum P-LAP (soluble), aminopeptidase A and post-proline endopeptidase, was studied by measuring liberated amino acids by high performance liquid chromatography. Placental particulate and soluble fractions degraded A-II almost completely into single amino acids. The purified P-LAP (microsomal) actively liberated five amino acids from the N-terminal. The placental particulate fraction containing P-LAP (microsomal) also actively liberated these amino acids. The purified aminopeptidase A liberated Asp1 very actively as expected. When the ratio of the velocity of liberation of each amino acid to P-LAP activity measured with leu-p-nitroanilide as a substrate was calculated, placental soluble fraction liberated Asp1 very actively, but the liberation rate of Asp1 with the purified P-LAP (soluble) was very low. Therefore it seems that the enzyme in the placental soluble fraction and pregnancy serum responsible for the Asp1 liberation is not P-LAP (soluble), but aminopeptidase A. The mixture of purified P-LAP (soluble) and aminopeptidase A showed higher liberation rate of Arg2 and Val3 than that with purified aminopeptidase A alone, demonstrating that once the N-terminal Asp1 was liberated, the P-LAP (soluble) attacks the shorter peptide (angiotension III) very actively. It was concluded that P-LAP (microsomal) together with aminopeptidase A seem to contribute greatly to the degradation of A-II in pregnant women.

Amino Acids↗

PubMed1976

[The ratio birth-weight, placental weight and the term of delivery. A contribution to the problem of a relative placental insufficiency in late pregnancy (author's transl)].

It is suggested, that a relative placental insufficiency in late pregnancy is one of the releasing factors of childbirth. Under this assumption 1027 deliveries in term pregnancy (266th-294th day of pregnancy) were inquired on the interrelationship between the ratio brith-weight: placental-weight and the duration of pregnancy. The average birth-weight increases slighly but significantly with the duration of pregnancy just as the average placental-weight. The average ratio birth-weight: placental-weight decreases significantly: The more unfavorable the ratio birth-weight: placental-weight is, the shorter remains the fetus in utero. This underlines the assumption of a relative placental insufficiency as one of the releasing factors of childbirth.

Birth Weight↗