Relationship between cortisol levels in umbilical cord plasma and development of the respiratory distress syndrome in premature newborn infants.

The aim of this study was to determine whether there is a decrease in fetal cortisol levels associated with the respiratory distress syndrome (RDS). Eighteen newborn infants of less than 37 weeks' gestation who developed moderate to severe forms of RDS did have a significantly lower (P less than 0.02) mean cord plasma cortisol concentration at birth than that observed in 67 unaffected infants of similar gestational age; mean values +/- standard errors were 3.36 +/- 0.42 and 5.58 +/- 0.43 mug per 100 ml, respectively. However, whether or not RDS developed in neonates appeared to depend more upon the degree of prematurity (with a 71.5% incidence in gestations of less than 32 weeks compared to 17.1% in those of 32 to less than 37 weeks) than upon cortisol levels at delivery. Bood cortisol levels in the first days of life of four infants with RDS were considerably increased in comparison to those at birth. Mean cord plasma cortisol concentrations increased with duration of pregnancy, with the previously observed value for term infants (of 37 or more weeks) being approximately twice that for infants of less than 32 weeks' gestation. These findings appear to justify carefully controlled studied with antepartum glucocorticoid administration with the aim of reducing the incidence of RDS in premature newborn infants.     

Evaluation of serum cortisol levels in a relatively large and mature group of ventilated and nonventilated preterm infants with respiratory distress syndrome

Severity of respiratory distress syndrome (RDS) and mechanical ventilation may affect the endogenous cortisol secretion in preterm infants. The aim of this study was to compare the serum cortisol concentrations of a relatively large and mature group of preterm infants with RDS who are ventilated or nonventilated and control preterm infants without RDS. Infants (group I) of comparable gestational ages without RDS served as controls. Infants with RDS who did not need ventilator support and surfactant therapy were considered to have mild RDS (group II). Those requiring mechanical ventilation and surfactant therapy were considered to have severe RDS (group III). Serum cortisol levels were determined after birth and on day 3 of life. The study groups consisted of 79 preterm infants with gestational ages ranging from 31 to 36 weeks, and birthweights ranging from 1086 to 1685 g. All preterm infants showed high cortisol levels after delivery regardless of respiratory distress (group I, n = 25, 34.1 +/- 10.7 microg/dL; group II, n = 23, 33.6 +/- 12.0 microg/dL; and group III, n = 31, 36.4 +/- 12.3 microg/dL). In group III, the cortisol levels (50.8 +/- 16.8 microg/dL) were higher than in group II (40.4 +/- 10.5 microg/dL) and in controls (22.0 +/- 7.2 microg/dL), and the cortisol levels of controls were lower than in group II on day 3 of life. Although the cortisol levels in severe and mild RDS infants increased significantly from their corresponding levels on day 1, they decreased in controls. The cortisol levels on day 3 of life were not significantly different in infants with poor outcome compared with infants with better outcome. Severity of RDS and mechanical ventilation were related to serum cortisol levels of preterm infants. Our study suggests that large and mature preterm infants who are ventilated and/or more severely ill release more cortisol than those less severely ill.     

Sex differences in correlation coefficient among the cord serum levels of LH-hCG, beta-hCG, FSH, estradiol cortisol and testosterone (author's transl)

Lutenizing hormone (LH-hCG), follicle stimulating hormone (FSH), beta-human chorionic gonadotropin (beta-hCG), estradiol, cortisol and testosterone were determined and correlated with each hormones in 62 cord sera (32 male and 35 female infants). Mean (+/- S.E.)male cord sera cortisol concentrations (36.2 +/- 3.9 ug/dl) were significantly (p less than 0.05) higher than that of female (24.1 +/- 3.7 ug/dl). Another hormones were not found significant sex difference. Regression analysis showed significant positive correlations between LH-hCG (r = 0.525, p less than 0.001) or beta-hCG (r = 0.461, p less than 0.005) levels and FSH levels in all cord sera (N = 67). In male cord sera, there were significant positive correlations between LH-hCG (r = 0.493, p less than 0.01) or beta-hCG (r = 0.485, p less than 0.01) levels and testosterone levels. There was a significant positive correlation (p less than 0.01) between estradiol levels and testosterone levels in female cord sera. These data suggest (1) the sex difference of cortisol levels which indicate the response for the stress during labor and delivery, (2) there was a significant sex difference in the maturation of the feed back mechanism in pituitary-gonadal axis.     

High incidence of respiratory distress syndrome (RDS) in infants born to mothers with placenta previa

OBJECTIVE: To evaluate the incidence of respiratory distress syndrome (RDS) in infants born to mothers with placenta previa and to assess the risk factors for RDS. METHODS: Ninety-nine pregnant women with placenta previa who delivered by cesarean section at 30-35 weeks of gestation were compared retrospectively with 102 pregnant women matched for week of gestation and birth year, who underwent elective cesarean section. Maternal characteristics, neonatal outcome, and incidence of RDS were analyzed. Umbilical cord blood samples were collected at delivery and were used to determine cortisol, epinephrine, and norepinephrine levels. Student's t-test, the chi-square test, and Fisher's exact test were used for statistical comparisons. P < 0.05 was considered significant. The Mann-Whitney U test was used for comparison of continuous variables. RESULTS: Preeclampsia, histological chorioamnionitis, and premature rupture of membranes were significantly lower in the placenta previa group (placenta previa: 2.0% vs. control: 14.7%, P < 0.01; 14.1% vs. 30.1%, P < 0.01; 7.1% vs. 17.6%, P < 0.05, respectively). The incidence of RDS was significantly higher in the placenta previa group than in the control group (29.3% vs. 6.9%, P < 0.0001). The cortisol level in umbilical cord blood in the placenta previa group was lower than in the control group (median 7.3, range 4.4-14.9 microg/dl vs. median 10.6, range 4.9-30.3 microg/dl, P < 0.05). There were no significant differences in epinephrine or norepinephrine levels between the two groups. CONCLUSIONS: The incidence of RDS in infants delivered at 30-35 weeks' gestation by cesarean section was significantly higher in mothers with placenta previa than in women without placenta previa. This may reflect decreased fetal stress since the cord blood cortisol levels were found to be lower in women with placenta previa.     

Management of women with one abnormal oral glucose tolerance test value reduces adverse outcome in pregnancy

In this study we sought to test the hypothesis that treatment of women with one abnormal oral glucose tolerance test value will result in reduction of adverse outcome. One hundred twenty-six women with one abnormal oral glucose tolerance test value and 146 women in the control group (normal oral glucose tolerance test values) participated in a prospective study during the third trimester of pregnancy. The subjects with one abnormal test result were randomized into treated (group 1) and untreated groups (group II). Group 1 subjects were treated with a strict diabetic protocol to maintain tight glycemic control by means of diet and insulin therapy. Group 2 subjects tested their capillary blood glucose for a baseline period. The study revealed that the level of glycemic control was similar before initiation of therapy (mean capillary blood glucose 118 +/- 14 vs. 119 +/- 15 mg/dl, p = NS) for groups 1 and 2, respectively. There was a significant difference in mean capillary blood glucose (95 +/- 10 vs. 119 +/- 15 mg/dl, p less than 0.0001), preprandial, and postprandial determinations between the treated and untreated groups. The overall incidence of neonatal metabolic complications (4% vs. 14%, p less than 0.05) and large infants (6% vs. 24%, p less than 0.03) was significantly lower in the treated group. Comparison between the control (normal oral glucose tolerance test) and the untreated groups showed a significantly higher incidence of large infants and metabolic complications. No difference was found between the normal and treated groups. Thus we conclude that treatment of individuals with one abnormal oral glucose tolerance test value will result in significant reduction in adverse outcome in pregnancy.     

Biologically active corticotropin-releasing hormone in maternal and fetal plasma during pregnancy

Corticotropin-releasing hormone was measured in the plasma of 110 pregnant women and in the umbilical cord plasma of 25 premature infants and 43 infants born at term. Mean maternal plasma corticotropin-releasing hormone was undetectable (less than 41 pg/ml) until mid-second trimester, rose to a mean of 204 +/- 24 pg/ml by 30 weeks' gestation, to 326 +/- 41 by 35 weeks, and then rose sharply near term, with a mean of 2930 pg/ml at 38 to 40 weeks' gestation. Sequential measurements in seven pregnant women confirmed that plasma corticotropin-releasing hormone rose in a predictable pattern, with a dramatic increase in the final weeks of pregnancy. There was little hour-to-hour variability in maternal plasma concentrations. Corticotropin-releasing hormone was also detectable in umbilical cord plasma; mean corticotropin-releasing hormone was 194 +/- 44 in the preterm infants and 150 +/- 19 in the term infants. The corticotropin-releasing hormone extracted from both the maternal and fetal circulation was biologically active in vitro and caused the dose-dependent release of adrenocorticotropic hormone and beta-endorphin from cultured rat anterior pituitary cells. A significant correlation was found between maternal plasma corticotropin-releasing hormone and cortisol levels the morning after betamethasone administration, a finding that supports a physiologic role for maternal plasma corticotropin-releasing hormone. We conclude that the placenta secretes large amounts of biologically active corticotropin-releasing hormone into both the maternal and fetal circulation during pregnancy. We demonstrate that this corticotropin-releasing hormone is secreted into the maternal plasma in a reproducible pattern during normal term pregnancy and suggest that sequential corticotropin-releasing hormone measurements may prove to be of clinical utility. In addition, placental corticotropin-releasing hormone may be an important modulator of the hypothalamic-pituitary-adrenal axis during pregnancy.     

Role of antioxidant nutrients and lipid peroxidation in premature infants with respiratory distress syndrome and bronchopulmonary dysplasia

The objective of this study was to determine if newborn premature infants with severe respiratory distress syndrome (RDS) who developed bronchopulmonary dysplasia (BPD) demonstrate, within the first 3 days of life, lower blood levels of antioxidants and higher urine levels of lipid peroxidation products than premature infants who recovered from RDS. Perinatal variables (gestational age, birth weight, and Apgar scores) and antioxidant indices in cord and in third day of life plasma and red blood cell (RBC) samples from healthy premature infants (n = 35), infants with RDS (n = 23) and infants with BPD (n = 23) were examined. Antioxidant indices included selenium, alpha-tocopherol, total and oxidized glutathione, glutathione peroxidase, superoxide dismutase, and urinary malondialdehyde. By inferential statistics, only the perinatal variables and cord plasma selenium distinguished healthy premature infants from premature infants with RDS or BPD. From perinatal variables and antioxidant indices we calculated: (1) cord to third-day-of-life variable differences, (2) variable-to-variable ratios, and (3) ratios of a difference for one variable to a difference for any second variable. Subset regression analysis yielded an equation (adjusted R2 = 0.8839) that correctly predicted infants who developed BPD 100% of the time. Predictor variables for BPD were gestational age, Apgar at 1 min, cord and third-day-of-life RBC selenium, cord total glutathione, cord and third-day-of-life glutathione peroxidase and nine different ratios involving Apgar scores, RBC selenium, total and oxidized glutathione, alpha-tocopherol, glutathione peroxidase, and superoxide dismutase. In this study, there was no relationship between lipid peroxidation and BPD. There was a higher rate of patent ductus arteriosus, congestive heart failure, and retinopathy of prematurity in infants with BPD. This study confirms that low plasma selenium and alpha-tocopherol levels in premature infants (< or = 30 weeks' gestational age or lower) were significantly associated with an increased respiratory morbidity.     

A double-blind study comparing ritodrine and terbutaline in the treatment of preterm labor

One hundred women in preterm labor were randomly treated with ritodrine or terbutaline in a double-blind fashion. The drugs were comparably effective during intravenous therapy but, in women with intact membranes, an oral dose of terbutaline, 30 mg daily, was significantly more effective than ritodrine, 120 mg daily, in preventing recurrent labor during a 5-day course of oral therapy (one of 19 versus 12 of 23, p less than 0.001). In women with intact membranes, pregnancy was prolonged 40 +/- 25 days (mean +/- SD) in women receiving terbutaline orally and only 22 +/- 24 days in women receiving ritodrine orally (p less than 0.01). In women with intact membranes, a heart rate greater than or equal to 130 bpm occurred in in a higher proportion of women receiving intravenous treatment with ritodrine than among those receiving terbutaline (20 of 31 versus 8 of 27, p less than 0.05). Terbutaline-treated women, however, were significantly more likely to have a serum glucose level in excess of 140 mg/dl than were women treated with ritodrine (13 of 26 versus 6 of 29, p less than 0.05). Side effects commonly observed during intravenous therapy included nausea (22%), chest pain (15%), and shortness of breath (15%). Side effects were significantly (p less than 0.025) more likely to occur during periods when the infusion rate was being increased rather than during periods when the infusion rate was constant.     

Postnatal changes in colloid osmotic pressure in premature infants: in healthy infants, in infants with respiratory distress syndrome, and in infants born to mothers with premature rupture of membranes

Colloid osmotic pressure (COP) of blood plasma during the first 4 days of life was measured in 63 neonates: 16 healthy preterm infants, 36 infants with respiratory distress syndrome (RDS), and 11 infants born to mothers with premature rupture of membranes. The relation between COP and total protein content of blood was significant in all groups over times from 1-3 h to 96 h. COP rose significantly by the age of 3 h compared to COP of umbilical cord plasma in all groups investigated. Infants with RDS showed a significant increase in COP during the investigation period. In healthy preterm infants the increase was less significant. In infants with RDS there was a negative correlation between changes in COP and body weight not seen in the other groups investigated. COP in neonates seems to reflect the compartmentation between vascular and interstitial spaces. Measurement of COP could be clinically useful in assessing hemodynamic adaptation after birth and also in assessing edema formation and water balance in infants with RDS.     

Apolipoprotein AI levels in cord blood]

Lipid is known to increase during pregnancy but the factors responsible for the change have not been established. In addition, the lipid concentration in preeclamptic pregnancy is significantly higher than in normal pregnancy. The apolipoproteins are an important determinant of metabolism and the structure of plasma lipoproteins. The 26 healthy pregnant women, the levels of cord apolipoprotein AI were determined by TIA methods. The cord and plasma apolipoprotein AI were 76.12 +/- 20.04 mg/dl (n = 26, mean +/- S.D.) and 190.50 +/- 18.84 mg/dl, respectively. Cord apolipoprotein levels correlated to maternal age (r = -0.12, p less than 0.05), maternal weight (r = -0.11, p less than 0.01), the gestational week (r = +0.42, p less than 0.01), infant weight (r = -0.01, p less than 0.05), placental weight (r = -0.03, p less than 0.05), and diastotlic blood pressure (r = +0.06, p less than 0.05). These data suggest that the measurement of cord apolipoprotein AI may be a useful factor in evaluating preeclamptic pregnancy.     

Cord serum lipid and apolipoprotein levels in preterm infants with the neonatal respiratory distress syndrome

Objective: The purpose of this study was to evaluate the effects of birth weight on cord serum lipid and apolipoprotein levels in preterm infants with and without respiratory distress syndrome (RDS). Methods: Cord serum lipid and apolipoprotein levels were evaluated in preterm infants (39 with RDS and 68 controls without RDS). Based on morbidity and mortality risk, RDS and non-RDS infants were separated into four birth weight groups (2000-2499 g, 1500-1999 g, 1000-1499 g, < 1000 g) and evaluated for effects of birth weight on cord serum levels. Results: RDS infants with birth weight of 2000-2499 g had significantly higher levels of cholesterol, triglyceride, total fatty acids and apolipoprotein A-I, but not arachidonic acid, than controls. RDS infants weighing 1000-1999 g had lower total fatty acids and apolipoprotein B levels, including arachidonic acid, than non-RDS infants. Cord serum lipid and apolipoprotein levels were significantly elevated in large (2000-2499 g) RDS infants, but lower levels were found in smaller (1000-1999 g) RDS infants. Conclusions: Cord serum arachidonic acid and apolipoprotein levels found in RDS infants suggest that lipid transport across the placenta may be abnormal. Inadequate total fatty acid supplies in utero could interfere with normal fetal growth and maturation, leading to development of neonatal RDS as one manifestation of risk for postnatal morbidity and mortality.     

Does intensive glycemic control in diabetic pregnancies result in normalization of other metabolic fuels?

Intensive treatment of insulin-dependent diabetes mellitus during pregnancy often normalizes plasma glucose levels. However, it is unclear whether this adversely affects other metabolic fuels that are essential to normal fetal growth and development. Metabolic studies were conducted after the subjects ingested a standardized mixed meal during each trimester in 7 normal and 15 insulin-dependent diabetic pregnant women. The latter were treated with continuous subcutaneous insulin infusion or multiple injections, which were adjusted to achieve strict glucose control throughout pregnancy. Insulin, alanine, branched-chain amino acids, triglycerides, free fatty acids, and ketones were measured every 15 to 30 minutes before a standardized breakfast and for 150 minutes after the breakfast. Patients with insulin-dependent diabetes mellitus were studied while they received their unusual insulin dosages. Fasting glucose levels (87 +/- 7 mg/dl) and glucose levels 150 minutes after the meal (112 +/- 11 mg/dl) were near normal. However, normoglycemia was achieved at the expense of increased plasma insulin levels (area under insulin response curves, p less than 0.01, vs nondiabetic curves). Nevertheless, fasting and post-prandial plasma branched-chain amino acids, alanine, and free fatty acids were similar in both groups. Fasting cholesterol, triglyceride, and ketone levels were also normalized. We conclude that normalization of circulating amino acids and lipids in conjunction with correction of hyperglycemia may contribute to favorable outcomes in infants of intensively treated diabetic mothers.     

Beta-mimetic drugs and possible prevention of respiratory distress syndrome.

The prophylactic value of beta-mimetic drugs in preventing respiratory distress syndrome (RDS) is investigated by comparing 29 preterm infants of ritodrine treated mothers with 34 preterm infants of a control group. Five cases of RDS (17 per cent) occurred among the infants of treated mothers as compared with 12 cases (35 per cent) in the control group (p = 0-09). The difference is, however, statistically significant for the group of infants weighing less than 2300 grams (p = 0-01) which includes all infants affected with RDS.     

Changes in thyroid status in newborn infants utero-exposed to ritodrine

A clinical study to assess whether utero exposure to ritodrine influences thyroid status was performed in 21 healthy term newborn infants, 10 exposed in utero to ritodrine (treated group) and 11 non-exposed in utero to drugs (control group). The treated group had a T3/T4 ratio significantly higher than the control group (mean +/- SD: 124.10 +/- 23.70 vs. 96.09 +/- 18.11, p less than 0.005) and T3 slightly increased (mean +/- SD nmol/l 2.48 +/- 0.69 vs. 1.95 +/- 0.56). The mean serum values of the other parameters studied, TSH, T4, fT4, fT3, were not significantly different in either groups. Since beta-mimetics induces deiodinating activity of the liver and propranolol reduces extrathyroidal conversion of T4 to T3, it was suggested that ritodrine enhances deiondinating activity of fetal and neonatal liver.     

Retrospective diagnosis of hypoxic myocardial injury in premature newborns

Perinatal asphyxia has a high impact on neonatal mortality, morbidity, and neurological outcome. The hypoxic effects on brain, kidney and gastrointestinal system are well recognized in newborns. While it is known that hypoxia also effects cardiac function, there are few studies of quantitative myocardial injury in premature infants who suffered hypoxia. AIM: To investigate usefulness of cardiac troponin (cTnT) and creatinine kinase MB (CK-MB) in the diagnosis of myocardial injury due to birth hypoxia and to correlate these markers with cardiac functions as measured by echocardiogram. METHODS: We studied 43 preterm infants: 21 with birth asphyxia and 22 controls. Echocardiographic studies and quantitative determination of cTnT and CK-MB in blood serum was performed between the 12(th) and the 24(th) h of life. RESULTS: cTnT and CK-MB levels were higher in asphyxiated infants compared to controls (0.287 +/- 0.190 vs. 0.112 +/- 0.099 ng/mL, P < 0.001) and (18.35 +/-14.81 vs. 11.09 +/- 5.17 ng/L, P < 0.05). Among controls, we observed an elevated value of cTnT in those with respiratory distress syndrome (RDS). We found a decrease in fractional shortening (P < 0.05) and an increase in tricuspid insufficiency (P < 0.01) in asphyxiated newborns. CONCLUSIONS: cTnT and CK-MB levels are strong indicators of myocardial injury due to perinatal hypoxia. The cTnT level was most strongly related to RDS.     

The physiologic hyperparathyroidism of pregnancy. Is it primary or secondary?

Controversy exists over whether the increase in maternal serum parathyroid hormone levels observed during the second half of pregnancy is due to autonomous parathyroid function or is secondary to changes in maternal serum ionized calcium levels. In order to study this problem further, 9 subjects were followed serially throughout normal pregnancy. Total serum calcium, ionized calcium, parathyroid hormone (PTH), calcitonin, and albumin levels were measured monthly. Six of these subjects had the studies repeated 6 weeks postpartum. Serum ionized calcium levels were found to decrease from 3.81 +/- 0.12 mg/dl to 3.63 +/- 0.18 mg/dl between 21 and 25 weeks' gestation. This decrease was significant at P less than 0.01. The ionized calcium remained in this lower range until term. A significant return to 3.77 +/- 0.1 mg/dl was observed 6 weeks postpartum. Serum PTH levels showed a significant rise after 21 weeks' gestation (P less than 0.05). No serial change in serum calcitonin was observed during pregnancy, although the mean level of the group was significantly higher than in nonpregnant controls (P less than 0.01). The increase in maternal serum PTH observed during pregnancy appears to be due in part to a decrease in maternal serum ionized calcium.     

Free carnitine levels in respiratory distress syndrome during the first week of life

Antenatal carnitine administration has been shown to induce fetal lung maturity by increasing pulmonary surfactant in animal and human studies. The aim of this study was to investigate serum free carnitine (FC) levels in preterm infants with respiratory distress syndrome (RDS) and controls during the first week of postnatal life. The study groups consisted of 76 preterm infants with gestational ages ranging from 28 to 36 weeks, and birthweights ranging from 1046 to 2352 g. Serum FC levels were measured in preterm infants (group A, 37 with RDS; group B, 39 controls without RDS) within the first 6 hours after birth, on days 3 and 7. For specific analyses, serum FC levels were determined for gestational ages 28 to 31 weeks and 32 to 36 weeks in both groups. Initial FC levels were decreased insignificantly in group A (22.5 +/- 7.3 micromol/L) compared with group B (23.5 +/- 6.8 micromol/L; P > 0.05). On days 3 and 7 of life, serum FC levels were significantly lower in group A (18.3 +/- 6.1 and 10.2 +/- 3.3 micromol/L, respectively) than in group B (23.4 +/- 7.1 and 22.8 +/- 3.7 micromol/L, respectively; P < 0.05 and P < 0.05, respectively) on days 3 and 7 of life, respectively. Serum FC level remained stable in the non-RDS group ( P > 0.05), but it decreased significantly in the RDS group during the first week of postnatal life ( P < 0.05). No differences were seen between the corresponding gestational age groups. Serum FC levels in RDS infants decreased from days 1 to 7. Decreased neonatal serum carnitine levels in preterm infants with RDS during the first week of life might be caused by increasing consumption of carnitine in lung tissue for surfactant synthesis.     

Maternal zinc and cord blood zinc, insulin-like growth factor-1, and insulin-like growth factor binding protein-3 levels in small-for-gestational-age newborns

PURPOSE: To determine the relationship between maternal serum zinc (Zn) levels and birth weight of the offspring and their correlation with cord blood Zn, insulin-like growth factor (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3) levels. METHOD: 22 term small-for-gestational-age (SGA) and 34 term appropriate-for-gestational-age (AGA) infants and their mothers were included. Maternal and cord blood Zn levels and cord blood IGF-1 and IGFBP-3 levels were measured. RESULTS: Eighteen percent of mothers had Zn deficiency (< 75 mcg/dl). No significant difference between IGF-1 and IGFBP-3 levels and birth weight of infants of the mothers with and without Zn deficiency was found. Maternal and neonatal Zn levels correlated (r = 0.38, p < 0.01). Mean IGF-1 and IGFBP-3 levels were significantly lower in the SGA group compared to the AGA group (42.3 +/- 16.8 ng/ml, 1.2 +/- 0.2 mcg/ml, and 62.4 +/- 22.7 ng/ml, 1.5 +/- 0.4 mcg/ml, p < 0.001). A correlation was found between birth weight, IGF-1 and IGFBP-3 levels, and weight gain of the mother during pregnancy (p < 0.01). CONCLUSIONS: Zn deficiency was not observed to be a risk factor for low birth weight. The significant difference between the SGA and AGA babies' IGF-1 and IGFBP-3 levels emphasizes function of the IGF system in intrauterine growth.     

Metabolic effects of intravenous ritodrine infusion during pregnancy

The effect of intravenous administration of ritodrine on blood glucose, insulin, free fatty acids and electrolytes in 17 third-trimester gravidas was investigated.A highly significant increase in blood glucose, insulin and free fatty acids and a marked decrease in serum potassium levels were registered. No significant changes during ritodrine infusion were recorded in serum levels of sodium, chloride, calcium, phosphorus and magnesium.No cardiac arrhythmias or electrocardiographic deteriorations occurred.While intravenous ritodrine administration seems to be safe in normal pregnancy, there may be a risk in diabetic patients, digitalized cases and those patients being treated with diuretics.     

Oxidative stress in pre-eclampsia

BACKGROUND: The objective of this study was to test the hypothesis that maternal plasma, cord plasma and placental tissue lipid peroxidation products are increased and antioxidants are decreased in women with pre-eclampsia. METHODS: Placenta, maternal and cord plasma were collected at delivery from 29 normal, 21 pre-eclamptic and six eclamptic women. Plasma was collected from 21 non-pregnant matched controls. The analyses were measured by HPLC and colorimetric assay. RESULTS: Plasma maternal concentrations of uric acid, LPO, MDA, ascorbic acid, vitamin E and cholesterol were not significantly different in pre-eclampsia as compared with normal pregnancy. Plasma concentrations of ascorbic acid and vitamin E were not significantly different in normal pregnancy as compared with the non-pregnant controls. Cord plasma concentrations of MDA were significantly higher in eclampsia (1.16+/-0.26 micromol/l) as compared with normal pregnancy (0.79+/-0.05 micromol/l, p<0.02) and pre-eclampsia (0.83+/-0.05 micromol/l, p<0.05). Cord plasma concentrations of vitamin E were significantly higher in eclampsia (21.3+/-7.5 micromol/l) as compared with normal pregnancy (10.2+/-1.1 micromol/l, p<0.01) and pre-eclampsia (10.4+/-1.8 micromol/l, p<0.04). Placental concentrations of LPO, MDA and ascorbic acid were not significantly different in pre-eclampsia as compared with normal pregnancy. Plasma cord concentrations of LPO and placental concentrations of vitamin E were undetected for normal pregnant, pre-eclamptic and eclamptic women respectively. Uric acid concentrations were significantly increased in eclampsia as compared with the non-pregnant controls (p<0.0001), normal pregnant controls (p<0.0001) and pre-eclampsia (p<0.008). CONCLUSIONS: The findings in this study do not show any evidence of deficiency in the maternal protective antioxidant systems or increased production of lipid peroxidation products, LPO and MDA in African women with pre-eclampsia as compared with normal pregnancy. However, there was evidence of increased cord plasma concentrations of MDA and vitamin E in eclampsia as compared with normal pregnancy and pre-eclampsia. The placenta may be effective in removing MDA. The antioxidant uric acid serves as a protective role whilst the antioxidant and oxidant capacity in the different study groups remained unchanged.