dinoprost has been researched along with Respiratory-Distress-Syndrome--Newborn* in 5 studies
1 trial(s) available for dinoprost and Respiratory-Distress-Syndrome--Newborn
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Prophylaxis of respiratory distress syndrome in premature calves by administration of dexamethasone or a prostaglandin F2 alpha analogue to their dams before parturition.
To investigate effects of preterm induction of calving by administration of flumethasone and dinoprost on the lecithin-to-sphingomyelin ratio in amniotic fluid and on neonatal respiratory distress after birth.. 45 dairy cows and their newborn calves.. Amniotic fluid from 45 cows was obtained and tested between days 258 and 270 of gestation. Cows were then given flumethasone (10 mg; n = 15), dinoprost (25 mg; n = 15), or saline solution (n = 15). Thirty hours later, left flank cesarean section was performed, amniotic fluid was collected, and the calf was delivered. Blood for determination of progesterone was withdrawn at amniotic fluid sample collections and before induction of calving. Blood for analysis of pH and base deficit was collected from calves during cesarean section and repeatedly after birth. Phospholipids in amniotic fluid were measured by thin-layer chromatography, and progesterone was determined by radioimmunoassay. Base deficit and pH were measured, using a blood gas analyzer.. Before treatments, a corpus luteum was present in all cows and the lecithin-to-sphingomyelin ratio in amniotic fluid did not differ between groups. Thirty hours after injections of flumethasone and dinoprost, progesterone concentration had decreased (P < 0.05) and the lecithin-to-sphingomyelin ratio was significantly (P < 0.05) higher than values in controls. In calves delivered after flumethasone or dinoprost treatments, the degree of acidosis was significantly (P < 0.05) less than that in controls.. Flumethasone and dinoprost, given to pregnant cows, accelerate fetal lung maturation and improve respiratory function after birth. Topics: Acidosis; Amniotic Fluid; Analysis of Variance; Animals; Animals, Newborn; Cattle; Cattle Diseases; Chromatography, Thin Layer; Dexamethasone; Dinoprost; Female; Flumethasone; Humans; Hydrogen-Ion Concentration; Incidence; Infant, Newborn; Injections, Intramuscular; Lung; Obstetric Labor, Premature; Phosphatidylcholines; Pregnancy; Progesterone; Radioimmunoassay; Respiratory Distress Syndrome, Newborn; Sphingomyelins; Time Factors | 1997 |
4 other study(ies) available for dinoprost and Respiratory-Distress-Syndrome--Newborn
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Eight-epi-PGF2alpha: a possible marker of lipid peroxidation in term infants with severe pulmonary disease.
A prostaglandin F2-like compound, 8-epi-PGF2alpha, formed from oxidation of arachidonate, has been proposed as an indicator of lipid peroxidation. We determined whether tracheal aspirate or urinary 8-epi-PGF2alpha levels would differ over time or between infants in a control group and infants with severe respiratory failure. We correlated tracheal aspirate 8-epi-PGF2alpha levels with the fraction of inspired oxygen and with mean airway pressures at 24 and 48 hours of life. Levels in tracheal aspirates were in the range of 0 to 36 pg/microg of fSC of IgA and were higher in infants with severe pulmonary disorders compared with those in infants in the control group (p < 0.02). Urinary concentrations did not discriminate between sick infants and infants in the control group. Topics: Biomarkers; Dinoprost; Exudates and Transudates; F2-Isoprostanes; Humans; Immunoenzyme Techniques; Infant, Newborn; Lipid Peroxidation; Lung Diseases; Respiratory Distress Syndrome, Newborn; Trachea | 1998 |
[The role of prostaglandins in pathogenetic mechanisms of the respiratory distress syndrome in premature newborn infants].
Topics: 6-Ketoprostaglandin F1 alpha; Dinoprost; Humans; Infant, Newborn; Lung; Prostaglandin Antagonists; Prostaglandins E; Respiratory Distress Syndrome, Newborn | 1989 |
Urinary excretion rates of 6-keto-PGF1 alpha in preterm infants recovering from respiratory distress with and without patent ductus arteriosus.
Patency of the ductus arteriosus in preterm infants is mediated by vasodilating prostanoids; however, reliable methods to monitor prostanoid activity or production in preterm infants are lacking. We measured the excretion rates of major and characteristic urinary metabolites of prostacyclin (PGI2), PGE1, and PGE2, 6-keto-PGF1 alpha, and 7 alpha-hydroxy-5,11-diketotetranorprostane-1,16-dioic acid (PGE-M), respectively. Besides these parameters which reflect total body prostanoid turnover and production, the urinary levels of PGE2 and PGF2 alpha, the primary prostaglandins, were measured as an index of renal prostanoid synthesis. There were four study groups. One contained 11 thriving preterm infants; a second, six preterm infants with respiratory distress syndrome (RDS); a third, 30 preterm infants with RDS and patent ductus arteriosus (PDA); and a fourth, nine fullterm infants. All infants with RDS required artificial ventilation. There were no significant differences in PGE-M, PGE2, and PGF2 alpha excretion rates among the various groups; however, a significant increase of the 6-keto-PGF1 alpha excretion rates was observed in the groups of infants with RDS and with and without PDA (P less than 0.01 and P less than 0.02, respectively). Spontaneous (n = 2) or indomethacin-induced (n = 6) closure of PDA was associated with weaning from the respirator and a concomitant drop into the normal and subnormal range of the excretion rates of 6-keto-PGF1 alpha (P less than 0.01) and PGE-M (P less than 0.02). Topics: 6-Ketoprostaglandin F1 alpha; Alprostadil; Dinoprost; Dinoprostone; Ductus Arteriosus, Patent; Female; Humans; Indomethacin; Infant, Newborn; Male; Prostaglandins E; Prostaglandins F; Prostanoic Acids; Respiration, Artificial; Respiratory Distress Syndrome, Newborn | 1984 |
Plasma prostaglandin E2 and F2 alpha in preterm infants: association with respiratory distress syndrome and patent ductus arteriosus.
In order to determine if prostaglandin values correlate with gestational age, birth weight, postnatal age, or respiratory distress syndrome (RDS), we determined plasma prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) by specific radioimmunoassay in 34 samples from 27 preterm infants. Neither prostaglandin correlated with gestational age or with birth weight. PGF2 alpha decreased (p less than 0.3) with postnatal age. Values for PGF2 alpha and PGE2 in each sample varied together (p less than .01) but only PGF2 alpha increased (p less than .09) in infants with RDS. The highest PGF2 alpha values occurred in infants with severe RDS, including four infants with patent ductus arteriosus (PDA). In contrast, plasma PGE2 was not elevated in infants with RDS or PDA. Topics: Age Factors; Birth Weight; Dinoprost; Dinoprostone; Ductus Arteriosus, Patent; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Prostaglandins E; Prostaglandins F; Respiratory Distress Syndrome, Newborn | 1983 |