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Biomedical subjects

E Marinoni

Publications and source records attributed to E Marinoni.

At least 37 records · Page 2Linked to original sources
PubMed1998

Immunoreactive adrenomedullin in human fetoplacental tissues.

OBJECTIVE: Adrenomedullin is increased in maternal plasma in pregnancy and has been found in very high concentrations in amniotic fluid and umbilical plasma. To identify adrenomedullin-producing tissue in pregnancy we measured adrenomedullin concentration and distribution in fetoplacental tissues. STUDY DESIGN: By use of a specific radioimmunoassay we determined the concentrations of adrenomedullin and, by immunohistochemical studies, its localization and distribution in fetal membranes and placentas collected at elective cesarean section from 11 healthy pregnant women at term. RESULTS: The content of adrenomedullin in placentas (117.7 +/- 7.8 pg/mg wet tissue) and fetal membranes (168.7 +/- 2.3 pg/mg wet tissue) was similar to the adrenomedullin concentration in adrenal medulla (157.3 +/- 4.4 pg/mg wet tissue). Adrenomedullin staining appears to be greater in fetal membranes than in placentas and was localized in amnion and trophoblast cells. In term placentas positive staining was detected predominantly in extravillous trophoblast cells, although a few syncytiotrophoblast cells and endothelial cells of primary villi stained for adrenomedullin. CONCLUSION: This study provides evidence that is consistent with fetoplacental tissues as a site of synthesis or action of adrenomedullin during pregnancy.

Adrenomedullin↗
PubMed1998

Effect of betamethasone in vivo on placental corticotropin-releasing hormone in human pregnancy.

OBJECTIVE: The objective was to determine the effects of in vivo administration of prenatal betamethasone in patients at 26 to 35 weeks' gestation on corticotropin-releasing hormone concentrations in maternal and fetal plasma and amniotic fluid, and on corticotropin-releasing hormone localization in placenta and fetal membranes. STUDY DESIGN: A total of 49 pregnant women at risk for preterm delivery between 26 and 35 weeks' gestation were studied. Twenty-six patients received betamethasone (12 mg intramuscularly) for stimulation of fetal lung maturity. Cord blood, amniotic fluid, placental tissue, and fetal membranes were obtained from 22 of these patients at delivery by elective cesarean section at 33.8+/-2.4 weeks' gestation. In control patients (n=23) at comparable gestational age, blood samples were taken for hormone analysis (n=8), and cord blood, amniotic fluid, and tissues were collected at elective cesarean section at 34.1+/-2.3 weeks' gestation. Concentrations of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol were determined by radioimmunoassay. Localization of tissue immunoreactive corticotropin-releasing hormone was assessed by immunohistochemistry. RESULTS: Betamethasone caused approximately 90% reduction in maternal cortisol and 50% reduction in maternal plasma adrenocorticotropic hormone. In patients at >30 weeks' gestation, there was a significant increase in maternal plasma corticotropin-releasing hormone concentrations after betamethasone; maternal corticotropin-releasing hormone was not altered significantly in untreated patients. Corticotropin-releasing hormone levels were raised in umbilical cord blood by 48 hours and in amniotic fluid 1 week after betamethasone administration. There was increased immunohistochemical staining for corticotropin-releasing hormone in placental syncytiotrophoblast and in fetal membranes of patients treated with betamethasone. CONCLUSIONS: These studies provide the first evidence for in vivo stimulation of plasma corticotropin-releasing hormone, likely of placental origin, by glucocorticoids in third trimester human pregnancy. The results suggest that increases in endogenous cortisol during normal gestation may contribute to placental corticotropin-releasing hormone output and to the rise in maternal plasma corticotropin-releasing hormone concentrations during late pregnancy.

Adrenocorticotropic Hormone↗
PubMed1998

Nitric oxide in preeclampsia: lack of evidence for decreased production.

The purpose of our study was to determine the involvement of the L-arginine-NO system in preeclampsia. We studied 26 patients with preeclampsia and 27 normotensive pregnancies. Maternal and cord plasma, urine and amniotic fluid were assayed for nitric oxide metabolites (nitrite and nitrate) using the Griess reaction. Sections of placenta and fetal membranes were immunostained with polyclonal anti-endothelial and anti-neuronal nitric oxide synthase antibodies. The concentration of nitrate in the amniotic fluid of preeclamptic patients (median 10.3 mumol/mg creatinine) was significantly higher (P < 0.001) than in the normotensive group (5.6 mumol/mg creatinine). Nitrate concentrations in maternal and cord plasma and in urine were similar in the two groups. Endothelial cells of the villi of preeclamptic placentas showed a higher positivity in endothelial nitric oxide synthase immunostaining with respect to normotensive controls. Our results indicate that feto-placental NO production is not reduced in preeclampsia. In contrast, the increased concentrations of NO metabolites in amniotic fluid and the positive immunostaining of endothelial nitric oxide synthase in the placental villi suggest that the placental L-arginine-NO system is up-regulated in preeclampsia.

Adult↗
PubMed1998

Antenatal glucocorticoid administration increases corticotrophin-releasing hormone in maternal plasma.

OBJECTIVE: This study was designed to determine whether maternal corticotrophin-releasing hormone (CRH) concentrations are altered after maternal betamethasone administration for fetal lung maturity in women with threatened preterm labour and whether these effects are dependent on gestational age. METHODS: Our study included 49 women with threatened preterm labour who received prenatal betamethasone for fetal lung maturity between 24 and 31 weeks of gestational age and 11 women who did not. Maternal blood was taken before and after glucocorticoid administration or at 24 hours after initial sampling. Plasma CRH, adrenocorticotrophin (ACTH) and cortisol concentrations were determined by radioimmunoassays. The women were stratified into 24-25 weeks, 26-27 weeks, 28-29 weeks, and 30-31 weeks completed gestation. RESULTS: At each gestational age, maternal cortisol concentrations decreased by approximately 85% after glucocorticoid administration. Overall mean cortisol values fell from 580.0 (SD, 351.8) to 89.7 (96.6) nmol/L (n = 40, P < 0.001). Overall mean ACTH values decreased from 9.9 (4.7) to 5.0 (3.4) pmol/L (n = 43, P < 0.001), and the approximate 50% decrease was similar at each gestational age. In marked contrast, overall mean CRH values increased from 58.0 (37.0) to 87.8 (68.6) pmol/L (n = 49, P < 0.001) after betamethasone administration. There was no change in maternal cortisol, ACTH or CRH values over 24 hours in women who did not receive betamethasone. CONCLUSIONS: We conclude that maternal betamethasone administration increases maternal plasma CRH values between 24 and 31 completed weeks of gestation.

Adrenocorticotropic Hormone↗
PubMed1998

Adrenomedullin, a new vasoactive peptide, is increased in preeclampsia.

Adrenomedullin is a novel peptide that elicits a long-lasting vasorelaxant activity. Recently, we found high concentrations of adrenomedullin in maternal and umbilical cord plasma and in amniotic fluid in full-term human pregnancy, indicating a role of this peptide during gestation. To investigate the possibility that adrenomedullin is involved in the pathophysiology of preeclampsia, we measured its concentration in maternal and fetoplacental compartments. We studied 12 normotensive nonpregnant women, 13 hypertensive nonpregnant subjects, 29 patients with preeclampsia, and 30 normotensive pregnant women. In all patients, plasma was collected from the cubital vein, and amniotic fluid samples were obtained by transabdominal amniocentesis or at elective cesarean section. Plasma samples from umbilical vein and placental tissues were collected at delivery. Adrenomedullin was assayed on plasma and amniotic fluid samples using a specific radioimmunoassay, and its localization and distribution on placental sections was determined by immunohistochemistry. Adrenomedullin concentrations were higher in hypertensive than in normotensive nonpregnant patients. Pregnant women had higher adrenomedullin levels than nonpregnant subjects, although maternal plasma adrenomedullin concentrations did not differ between normal pregnant and preeclamptic women. Preeclamptic patients showed higher concentrations (P<0.01) than normotensive pregnant women of adrenomedullin in amniotic fluid (252+/-29 versus 112+/-10 fmol/ micromol creatinine) and umbilical vein plasma (18.1+/-2.1 versus 8. 5+/-1.1 fmol/mL). Increased local production of adrenomedullin is associated with preeclampsia. The fetus seems to be responsible for the higher levels of this hormone. Increased adrenomedullin concentrations may be necessary to maintain placental vascular resistance and/or fetal circulation at a physiological level.

Adrenomedullin↗
PubMed1998

New peptides, hormones and parturition.

This brief review emphasizes the importance of three novel discovered factors produced by fetal membranes, placenta and/or by the fetus itself in regulating uterine contractility. We have shown that, as reported for other hormones and substances, nitric oxide and endothelin may influence myometrial activity in an autocrine/paracrine manner interacting with other well-known agents such as prostaglandins, oxytocin and hormones. We also demonstrated that different isoforms of nitric oxide synthase (NOS) may play different roles throughout gestation and during labor. We have suggested that another peptide produced by trophoblast cells, adrenomedullin, may affect, directly or indirectly, myometrial contractility during pregnancy, although much remains to be learned about the mechanisms controlling adrenomedullin expression by the feto-placental tissues cells during pregnancy. Continued research is necessary to better define the complex interactions that result in parturition, both at term and preterm, and to allow a more rational approach to management of the premature labor, exploring new possible pharmacological solutions.

Adrenomedullin↗
PubMed1997

Amniotic fluid nitric oxide and uteroplacental blood flow in pregnancy complicated by intrauterine growth retardation.

OBJECTIVE: To examine the correlation between placental nitric oxide production and uteroplacental blood flow. PARTICIPANTS: Thirty-one pregnant women with fetuses with intrauterine growth retardation and 27 normal pregnancies as controls. DESIGN: Correlation between amniotic fluid measurements of nitrite metabolite in the third trimester and flow velocimetry waveforms recorded from uterine, umbilical and fetal middle cerebral arteries. Intrauterine growth retarded pregnancies were compared with controls. MAIN OUTCOME MEASURES: Concentrations of nitric oxide metabolites (NO2- and NO3-) in amniotic fluid were correlated with flow velocimetry waveforms findings by the determination of correlation coefficient. RESULTS: Overall median nitrite values in amniotic fluid were higher (P < 0.01) in intrauterine growth retarded patients (median 8.6 micromol/mg creatinine) than in controls (5.6 micromol/mg creatinine). Pathologic uterine flow velocimetry waveforms in uterine artery (-2SD) were observed in 12 women of the intrauterine growth retarded group, and the concentration of amniotic fluid nitrite was significantly lower (P < 0.01) in these patients (median 4.45 micromol/mg creatinine) than in those with normal flow velocity waveforms (median 11.43 micromol/mg creatinine). A significant negative correlation was observed between nitrite concentrations and uterine artery resistance index, umbilical artery pulsatility index and umbilical artery pulsatility index:middle cerebral artery pulsatility index ratio. CONCLUSIONS: We conclude that placental nitric oxide is significantly associated with uteroplacental blood flow and may be important in maintaining adequate uteroplacental perfusion in intrauterine growth retarded pregnancies.

Adult↗
PubMed1997

Immunohistochemical localization of nitric oxide synthase in human fetal membranes.

SUBJECT: It has been demonstrated that L-arginine-nitric oxide (NO) system is present in the myometrium during pregnancy where it can regulate uterine contractility. MATERIAL AND METHOD: We have studied by immunohistochemistry the localization of constitutive endothelial nitric oxide synthase (ecNOS) and brain nitric oxide synthase (bNOS) in human fetal membranes in term non laboring women. RESULTS: The amniotic epithelium and the trophoblast of chorion layer stained intensively for bNOS, while for ecNOS the immunoreactivity was weak and restricted to trophoblast cells. CONCLUSION: These findings are suggestive for NO production by the fetal membranes in term pregnancy.

Extraembryonic Membranes↗
PubMed1996

Amniotic fluid endothelin-1 levels are increased in pregnancy-induced hypertension and intrauterine growth retardation.

Endothelin-1 (ET-1) is a potent vasoconstrictor released by vascular endothelium. Because endothelial cell damage is considered determinant in the pathophysiology of pregnancy-induced hypertension (PIH), this study was conducted to evaluate the role of ET-1 produced by feto-placental tissues in PIH. Amniotic fluid samples obtained by amniocentesis from patients with PIH (N = 33), intrauterine growth retardation (IUGR) (N = 16), and PIH associated with IUGR (N = 12) were evaluated for ET-1 and compared to 42 normotensive pregnancies using a specific radioimmunoassay. ET-1 levels were significantly increased in PIH (35.6 +/- 1.9 pg/ml) and IUGR groups (33.8 +/- 4.6 pg/ml) compared to controls (20.8 +/- 1.4 pg/ml) (P < 0.01). In patients with PIH associated with IUGR, ET-1 concentrations were higher (P < 0.05) with no correlation with the severity of IUGR. Our data indicate that in PIH and IUGR ET-1 production and/or secretion is enhanced in the amniotic compartment, suggesting that the peptide may contribute to the pathophysiologic modification observed in these conditions.

Adult↗
PubMed1995

Immunohistochemical localization of endothelin-1 in placenta and fetal membranes in term and preterm human pregnancy.

PROBLEM: The aim of the study was to determine the ET-1 localization on human placenta and fetal membranes and to compare its distribution between term and preterm pregnancies in laboring and non-laboring tissues. METHODS: Tissues obtained from nine term elective cesarean section, eight spontaneous vaginal term delivery, and 13 preterm delivery from both cesarean section (N = 6) and vaginal delivery (N = 7) were studied by immunohistochemistry. RESULTS: Immunoreactive ET-1 (IR-ET-1) was detected in villous and nonvillous trophoblast in all groups, although laboring tissues showed strong staining in the syncytiotrophoblast of the villi. ET-1 immunostaining of endothelial cells was observed in all placental villous vessels with a considerable variability within groups. In the fetal membranes, intensive immunopositive staining was observed in the chorionic trophoblast following vaginal deliveries in term and preterm tissues. CONCLUSIONS: This is the first study to report the localization of IR-ET-1 in human fetal membranes and placenta, and suggests that amnion and trophoblast represents a source of ET-1 production or, alternatively, a site for ET-1 binding.

Endothelins↗
PubMed1995

Sympathetic modulation of radial artery compliance in congestive heart failure.

Animal studies have suggested that arterial compliance can be modulated by adrenergic influences. Whether this adrenergic modulation also occurs in humans is still a matter of debate. In the present article we address this issue by examining the relationships between sympathetic tone and arterial compliance in a variety of physiological and pathophysiological conditions. We have found that cigarette smoking, ie, an action that produces a marked sympathetic activation, causes a significant reduction in radial artery compliance, as measured by an echotracking device capable of providing continuous beat-to-beat evaluation of this hemodynamic variable. When expressed as compliance index, ie, as the ratio between the area under the compliance-pressure curve and pulse pressure, the reduction amounted to 35.7 +/- 4.8% (mean +/- SEM) and was independent of the smoking-related blood pressure increase. Furthermore, pharmacological stimulation of adrenergic receptors located in the arterial wall was also shown to affect arterial compliance because the radial artery compliance index was markedly reduced (- 29.5 +/- 3.9%) during phenylephrine infusion in the brachial artery at doses devoid of any systemic blood pressure effect. Evidence was also obtained that the relationship between sympathetic activation and arterial compliance has pathophysiological relevance, because in 17 patients with congestive heart failure (New York Heart Association classes II through IV) there was a significant inverse correlation (r = .62, P < .01) between muscle sympathetic nerve activity (directly measured by microneurography in the peroneal nerve) and radial artery compliance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Cell-mediated immunity imbalance in pregnancy-induced hypertension.

Pregnancy is associated with modifications in the maternal immune system that may be involved in the absence of rejection of the fetoplacental graft characterized by the presence of paternal antigens. This active and specific tolerance towards the fetoplacental unit seems to be compromised in pregnancy-induced hypertension (PIH). To evaluate whether the immunological state in patients with PIH is altered with respect to normal pregnant women we studied 15 patients with PIH, 15 uncomplicated pregnant and 10 healthy nonpregnant women using monoclonal antibodies directed to specific lymphocyte antigen determinants, cytokines (TNF) and soluble molecules (sIL-2R, sCD8). The percentage of CD4 lymphocytes and of natural killer (NK) cells was significantly higher in PIH patients compared to controls (CD4: 42.9 +/- 10.5 vs. 32.7 +/- 12.5%; p < 0.05; NK: 14.7 +/- 6.3 vs. 8.3 +/- 3.4%; p < 0.01). However, these values did not differ when compared to normotensive nonpregnant controls (CD4: 53.1 +/- 5.9%; NK: 17.2 +/- 7.1%). In addition, the soluble IL-2 receptor (sIL-2R) was higher in PIH patients when compared to control patients (725.5 +/- 194.2 vs. 482.5 +/- 187.2 U/ml; p < 0.01). The immune response observed in normal pregnancies responsible for the tolerance towards the fetoplacental unit seems to be altered in PIH patients as suggested by higher levels of CD4 and NK cells, and sIL-2R. This may lead to a chronic rejection syndrome and be involved in the pathophysiology of PIH.

Adolescent↗
PubMed1987

[Unusual cause of post-traumatic hemoperitoneum: rupture of enterogenous cysts].

Authors present a rare complication of multiple enteric cystes: hemoperitoneum. A little girl 4 years old was operated on by suspected acute appendicitis. The surgery showed hemoperitoneum by bleeding from broken (post-traumatic) paradigiunal cyst. Other 5 cystes were present near the first one. Authors review shortly some titles of bibliography about duplication of the alimentary tract and hemoperitoneum.

Accidental Falls↗