Search PubMed⌕ Search

Biomedical subjects

U Ekblad

Publications and source records attributed to U Ekblad.

49 records · Page 3Linked to original sources
PubMed1988

Ritodrine infusion at term: effects on maternal and fetal prostacyclin, thromboxane and prostaglandin precursor fatty acids.

A prospective randomized study was performed to investigate the effect of a short-term ritodrine infusion on the concentrations of maternal and fetal prostaglandins and their precursor fatty acids. Mothers gave birth by an elective cesarean section at term, and either ritodrine (study group) or physiological saline (controls) was infused 2 h prior to the operation. Ritodrine decreased the levels of thromboxane A2 significantly in the mother, while the concentration of prostacyclin remained unchanged. In the umbilical arterial plasma concentrations of prostacyclin or thromboxane A2 there were no differences between ritodrine-treated and control subjects. Ritodrine had no effect on the prostaglandin precursor fatty acids and other fatty acids of plasma phospholipids of the mother or her fetus. It is concluded that ritodrine may suppress the maternal prostaglandin production, but has no effect on the levels of vasoactive prostaglandins or their precursor fatty acids in the fetus.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

The effect of acute hypoxia on prostaglandin release in perfused human fetal placenta.

The release of prostaglandin E2 and F2 alpha, thromboxane B2 and 6-keto-prostaglandin F1 alpha was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period, prostaglandin E2 accounted for 44% and 6-keto-prostaglandin F1 alpha for 28% of all prostaglandin release, and the rank order of prostaglandin release was E2 greater than 6-keto-prostaglandin F1 alpha greater than thromboxane B2 greater than prostaglandin F2 alpha. Hypoxia had no significant effect on quantitative prostaglandin release, but the ratio of prostaglandin E2 to prostaglandin F2 alpha was significantly increased. After the hypoxic period during reoxygenation the release of 6-keto-prostaglandin F1 alpha was significantly decreased, as was the ratio of 6-keto-prostaglandin F1 alpha to thromboxane B2. Also the ratio of the vasodilating prostaglandins (E2, 6-keto-prostaglandin F1 alpha) to the vasoconstricting prostaglandins (thromboxane B2, prostaglandin F2 alpha) was decreased during reoxygenation period. With the constant flow rate, the perfusion pressure increased during hypoxia in six and was unchanged in three preparations. The results indicate that changes in the tissue oxygenation in the placenta affect prostaglandin release in the fetal placental circulation. This may also have circulatory consequences.

Aerobiosis↗
PubMed1987

Effect of antepartum ritodrine on the cardiorespiratory status of the newborn after elective cesarean section.

Heart rate (HR), heart rate variability (HRV), respiratory rate (RR) and transcutaneous PO2 and CO2 of 12 infants born by elective cesarean section were monitored during the first postnatal hour in order to evaluate the effect of the beta-mimetic tocolytic drug ritodrine. Six of the mothers received ritodrine by infusion and the other 6 physiological saline during the 2 h prepartum. The Apgar scores of the treatment group were higher (p less than 0.05) but there was a significant increase in RR (p less than 0.05) during the first hour in these babies. Arterial blood pressure (BP) was lower in the group whose mothers had received ritodrine (p less than 0.05) but there was no difference in pulse pressure. Transcutaneous pressure of CO2 (PtcCO2) of the controls decreased during the first hour (p less than 0.05). Transcutaneous pressure of O2 (PtcO2) increased during the first postnatal hour (p less than 0.01) when both groups were examined together. HR of both groups was relatively high and HRV low.

Carbon Dioxide↗
PubMed1987

The effect of a short-term ritodrine treatment on the concentration of beta-adrenergic receptors in human myometrium.

The concentration of beta-adrenoceptors in human myometrium has been studied of women giving birth by elective cesarean section at term. Eight of the woman were treated with intravenous ritodrine two hours prior to the operation. In the control group seven women received physiological saline with the same infusion rate as ritodrine in the study group. The concentration of beta-receptors in the myometrium of the lower uterine segment was determined with radioligand binding assay. Ritodrine treatment decreased the available beta-receptors significantly.

Female↗
PubMed1987

Intracervical prostaglandin E2 gel for cervical ripening.

Forty-five women with an unfavourable cervix (cervical score less than 3) and an obstetric indication for delivery were given intracervical prostaglandin E2 (PGE2) gel 0.5 mg/3 g to prime the uterine cervix. Twenty-one women (47%) went into labour after PGE2 gel application only. In 13 women (29%) the cervical score sufficiently improved within 12 hours and labour was successfully induced with intravenous oxytocin. The rate of adverse effects was notably: there were two uterine ruptures, the rate of cesarean sections was 33%, hypertonic uterine contractility 25%, premature rupture of membranes 16%, and neonatal asphyxia 21%. In our experience, cervical ripening with PGE2 gel, although efficient, may also bring about complications, which appear partly iatrogenic. Therefore, a critical evaluation of indications and the risk/benefit ratio is required.

Cervix Uteri↗
PubMed1987

HELLP syndrome.

HELLP syndrome is a triad of hemolysis, elevated liver enzymes and low platelet count during pregnancy and it is proposed to be a sign of severe preeclampsia. We present two mothers with this life-threatening condition. In the first case, the syndrome appeared after a twin delivery at 34 weeks of pregnancy. The mother required 10 days of intensive care with blood and thrombocyte transfusions. Both she and the infants survived. In the second case, the mother had all classic signs of severe preeclampsia at the 27 week of pregnancy. After 3 days' intensive care, a cesarean section was performed and both the mother and the child survived.

Adult↗
PubMed1986

The effect of oxytocin and betamimetic stimulation on prostaglandin release in perfused human fetal placenta.

The existing data on prostaglandins indicate that they are involved in human parturition and regulation of fetoplacental blood flow. The interference of endogenous and exogenous oxytocin and prostaglandins and, on the other hand, betamimetics, which are commonly used during pregnancy, in the regulation of these phenomena is poorly understood. The production of prostaglandins by fetal placental cotyledons was studied using an in vitro perfusion technique. Isolated cotyledons were perfused without (control) or with oxytocin (200 pg/ml, 2000 pg/ml) or the betasympathomimetic drug ritodrine (10 micrograms/ml, 50 micrograms/ml). The release of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2) was measured by radioimmunoassay. The release of prostaglandins was also studied during a recovery period after the drug infusion. Oxytocin at a concentration of 200 pg/ml significantly decreased the release of PGF2 alpha. A higher concentration of oxytocin did not cause any changes in prostaglandin production. During ritodrine infusion the perfusion pressure was decreased, but the addition of ritodrine to the perfusion medium had no effect on prostaglandin release. During the recovery period, after ritodrine infusion, the release of PGF2 alpha was significantly decreased. It is suggested that oxytocin at the physiological concentration may protect the fetus from adverse effects of PGF2 alpha before labor in decreasing the release of PGF2 alpha, yet this small decrease in formation of PGF2 alpha is obviously of minor clinical importance because the perfusion pressure remained constant. Ritodrine had no effect on prostaglandin release and so the decrease in the perfusion pressure is probably the result of beta 2-receptor stimulation.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Serum prostaglandin precursors after vaginal examination and amniotomy.

The effect of vaginal or cervical examination during pregnancy upon the levels of circulating prostaglandin precursors and other free fatty acids was investigated. Of 31 mothers coming to elective induction of labor, a plain vaginal examination was performed in 9 cases, the cervix was penetrated by a finger and the membranes were slightly swept off the uterine wall in 10 cases and an amniotomy was performed in 12 cases. The blood samples were collected before and 5 minutes after the procedure. No changes were observed in prostaglandin precursors or in other free fatty acid levels. Also the precursors/other fatty acids ratio was unchanged. The demonstrated changes in circulating prostaglandin levels after these procedures are not reflected in the circulating precursor levels.

Amnion↗
PubMed1984

Composition of free fatty acids at the end of pregnancy and inducibility of labor.

The concentrations of free fatty acids which included prostaglandin precursors were investigated in a group of 54 healthy women coming to elective induction of labor. There were no differences between the concentrations of the fatty acids when the mothers were divided in two groups according to whether induction was successful or not. There were slightly more mothers with successful induction, who had the total prostaglandin precursor level above average than among mothers with unsuccessful induction (p less than 0.05). The rates of false positives or false negatives were so high, however, that this determination can not be clinically used in predicting the outcome of labor induction.

Arachidonic Acids↗
PubMed1984

Metabolism of prostaglandin F2 alpha in the fetal circulation of the human term placenta in vitro.

The metabolism of prostaglandin F2 alpha (PGF2 alpha) was investigated in the fetal cotyledons of human term placentas by an in vitro perfusion technique. When 80 nmol of 14C-PGF2 alpha was infused in 2 min into the chorionic artery, 56 +/- 7% (mean +/- SEM, n = 7) of the infused radioactivity appeared in the nonrecirculating venous effluent in 6 min. Most of this radioactivity was as unmetabolized PGF2 alpha. Only 12 +/- 2% of the radioactivity in this venous effluent was as metabolites, the major metabolite being 13,14-dihydro-15-keto-PGF2 alpha. During the following 2 min, 2 +/- 1% of the infused radioactivity appeared in the venous effluent. The fluid trickling through the decidual plate contained 5 +/- 1% of the infused radioactivity. After the perfusion 10-15% of the infused radioactivity was retained in the tissue, being mainly as 13,14-dihydro-15-keto-PGF2 alpha. The oxygen consumption of the tissue was 0.4 +/- 0.1 ml/100 g/min, which is adequate for vital placenta tissue. The study suggests that the metabolism of PGF2 alpha is negligible in the fetal circulation of the human term placenta.

Dinoprost↗
PubMed1982

Prostaglandin E2 is only slightly metabolized in the fetal circulation of perfused human placenta.

The metabolism of prostaglandin E2 (PGE2) was investigated in the fetal circulation of one cotyledon or a group of cotyledons in human term placentas by in vitro perfusion technique. When 100 nmol of 14C-PGE2 was infused in 2.5 minutes into the chorionic artery, 75 +/- 5% (mean +/- SEM, n=8) of the infused radioactivity appeared in the nonrecirculating venous effluent in six minutes. Most of the radioactivity was in the fraction of unmetabolized PGE2, only 6-13% of the radioactivity in the effluent appeared in metabolite fraction, the major metabolite being 14-keto-13,14-dihydro-PGE2. The amount of metabolites in 0-6 min effluent was 0.13 +/- 0.01 nmol/g of perfused placenta. This rate of formation of PGE2 metabolites is very low compared to the activity of NAD+-dependent 15-hydroxyprostaglandin dehydrogenase, which was 183 +/- 19 nmol x min-1 x g of tissue-1 (n=5) when measured from the 100.000 g supernatant fraction of homogenized human placenta using 14C-PGE2 as the substrate. The present study indicates that PGE2 is only slightly metabolized in the fetal circulation of human placenta, in spite of high activity of 15-hydroxyprostaglandin dehydrogenase in placental tissue.

Arteries↗