Maurizio M. Anceschi

Beta-adrenergic stimulation of prostaglandin production by human amnion tissue

Arachidonic acid is released from specific glycerophospholipids in human amnion and is used to synthesize prostaglandins that are involved in parturition. In an investigation of the regulation of prostaglandin production in amnion, the effects of isoproterenol on discs of amnion tissue maintained in vitro were examined. Isoproterenol caused a large but transitory increase in the amount of cyclic AMP in amnion discs and this was accompanied by a sustained stimulation of the release of arachidonic acid (but not palmitic acid or stearic acid) and prostaglandin E2. The dependencies of cyclic AMP accumulation, arachidonic acid mobilization and prostaglandin E2 release on the concentration of isoproterenol were similar, each response was maximal at 10(-6) M isoproterenol and was inhibited by propranolol. Dibutyryl cyclic AMP stimulated the release of prostaglandin E2 from amnion discs. Although prostaglandin E2, when added to amnion discs caused an accumulation of cyclic AMP, it did not appear to mediate isoproterenol-induced accumulation of cyclic AMP since the latter effect was insensitive to indomethacin in concentrations at which prostaglandin production was inhibited greatly. These data support the proposition that catecholamines, found in increasing amounts in amniotic fluid during late gestation, may be regulators of prostaglandin production by the amnion.

Deficiency of human placental lactogen in an otherwise normal pregnancy

SummaryWE report a further case of human placental lactogen (HPL) deficiency associated with a normal pregnancy. To our knowledge, this is the first case reported from Italy and the fifth in the literature (Gaede et al., 1978; Nielsen et al., 1979; Moshirpur et al., 1981; Borody and Carlton, 1981).

Maternal haemodynamic and haemorrheologic considerations in fetal I.U.G.R.

IUGR is a symptom which has many causes; genetic abnormalities, feto-maternal infections, maternal drug intake, smoking, socio-demographic factors, all are related to fetal IUGR, but the most common underlying cause is the inadequate or inappropriate placental function. This is obvious because placenta plays a central role in fetal nutrition and there is no survival of the fetus in utero without the support of the placenta. The diminished fetal growth rate can be considered äs an intrauterine mechanism of defence against hypoxic damage, because in this way there is a saving of oxygen for the cerebral tissue.

Erythrocyte membrane composition in pregnancy‐induced hypertension: Evidence for an altered lipid profile

OBJECTIVE To investigate whether the increased membrane fluidity postulated as a possible contributing factor to the hypertensive states of pregnancy is related to the lipid composition of the erythrocyte membrane. DESIGN An observational case control study. SUBJECTS 30 women with pregnancy induced hypertension, 26 normotensive pregnant women matched for gestational age, and 10 normotensive non pregnant nulliparous women. INTERVENTIONS Erythrocyte membranes were prepared from venous blood samples obtained from all the women. MAIN OUTCOMES MEASURES Lipid analysis, including cholesterol to phospholipids ratio, distribution of phospholipid classes and fatty acid composition of total phospholipids in erythrocyte ghosts. RESULTS The cholesterol/phospholipid ratio was significantly higher in the women with pregnancy induced hypertension compared with the normotensive pregnant women (mean 1.24, SD 0.31, 95% CI 1.12 to 1.35 vs mean 0.90, SD 0.09, 95% CI 0.86 to 0.94; P less than 0.01). Normotensive non-pregnant erythrocyte membrane cholesterol/phospholipid ratio was 0.88 (SD 0.11, 95% CI 0.79 to 0.96). The percentage distribution of different phospholipid classes and fatty acid composition was similar in all the four groups. CONCLUSIONS The increased cholesterol/phospholipid ratio of the erythrocyte membrane found in pregnancy-induced hypertension represents one factor involved in the pathophysiology of this condition and a possible biochemical marker of the disease.

Effects of corticosteroids on fetal lung maturation

Several investigations and controlled trials have shown that antenatal administration of corticosteroids leads to a significant reduction in the occurrence of respiratory distress syndrome (RDS) and to an overall decrease in neonatal mortality among prematurely delivered infants [1,2]. The effects of corticosteroids on the fetal lung are multilayered and affect a number of aspects of lung maturation. In order to elucidate the mechanisms by which corticosteroids enhance fetal lung maturation, we examined the effects of antenatal administration of betamethasone on different properties of lungs from prematurely delivered rabbit neonates.

Regulation of Arachidonic Acid Release for Prostaglandin Production during Parturition

The sources of arachidonic acid for the production of prostanoids during early labor have been identified as (diacyl)phosphatidylethanolamine and phosphatidylinositol. The enzymatic mechanisms that account for the selective mobilization of arachidonic acid in amnion tissue from these two glycerophospholipids are described. Based on the activation/inhibition of the enzymes involved in these processes, we suggest a central role for \(C{{a}^{{{{2}^{ + }}}}}\) in the regulation of prostanoid biosynthesis in this tissue. Platelet-activating factor (PAF) has been identified in amniotic fluid from women in labor, in the urine and tracheal fluid of the newborn, and in amnion tissue. Increased PAF concentrations were found in the amnion tissue obtained at term from women in labor. PAF biosynthesis and hydrolysis has been demonstrated in amnion tissue. LysoPAF:acetylCoA acetyltransferase was activated by \(C{{a}^{{{{2}^{ + }}}}}\) at micromolar concentrations. A biochemical model for the regulation of arachidonic acid release and prostanoid formation in relation to parturition is presented.

Renin activity, aldosterone levels and urinary sodium and potassium excretion under tocolytic therapy with salbutamol.

The effects of long-term therapy with salbutamol on renin activity, aldosterone levels and urinary sodium and potassium excretion in pregnant women are studied. Salbutamol was given intravenously in a first group of 18 patients in preterm labor, orally in a second group of 9 patients, whereas a third group of 17 patients was taken as control. No significant changes were observed in renin activity and aldosterone levels between the first and the fifth day of intravenous or oral therapy and in 24-h sodium urinary excretion. Only potassium excretion showed a significant decrease (P less than 0.01) within 24 h from the start of the intravenous therapy, returning to control levels after 48 h. From these results, no replacement of potassium seems to be necessary in patients undergoing tocolytic therapy with betamimetic drugs.