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At least 217 records · Page 12Linked to original sources
PubMed1988

Transcatheter closure of a calcified patent ductus arteriosus in an elderly man.

Successful transcatheter closure of a calcified patent ductus arteriosus was performed in a symptomatic 78 year old man. Cardiac catheterization revealed a left to right shunt across the patent ductus arteriosus with a pulmonary to systemic flow ratio of 2.8:1. Calcification of the ductus and severe lung disease increased the risk of surgical patent ductus arteriosus closure. A 17 mm Rashkind double umbrella was positioned in the ductus percutaneously by way of the femoral vein. After closure of the ductus there was marked hemodynamic improvement and the patient was discharged with improved exercise tolerance. Transcatheter closure of patent ductus arteriosus may be a viable option for the elderly patient too sick to withstand cardiovascular surgery.

Aged↗
PubMed1996

Oxygen-induced constriction of rabbit ductus arteriosus occurs via inhibition of a 4-aminopyridine-, voltage-sensitive potassium channel.

The ductus arteriosus is a vital fetal structure allowing blood ejected from the right ventricle to bypass the pulmonary circulation in utero. Closure of the ductus arteriosus at birth, essential for postnatal adaptation, is initiated by an increase in oxygen (O2) tension. We recently demonstrated the presence of O2-sensitive potassium channels in the fetal and adult pulmonary circulation which regulate vascular tone in response to changes in O2 tension. In this study, we assessed the cellular mechanisms underlying O2-induced constriction of the ductus arteriosus in late-gestation fetal rabbits. We report that O2 reversibly inhibits a 58-pS voltage- and 4-aminopyridine-sensitive potassium channel, causing membrane depolarization, an increase in intracellular calcium through L-type voltage-gated calcium channels, and constriction of the ductus arteriosus. We conclude that the effector mechanism for O2 sensing in the ductus arteriosus involves the coordinated action of delayed rectifier potassium channels and voltage-gated calcium channels.

4-Aminopyridine↗
PubMed2001

Effect of gestational age, corticosteroids, and birth on expression of prostanoid EP receptor genes in lamb and baboon ductus arteriosus.

The aim of this study was to determine the effect of corticosteroids, gestational age, and birth on the expression of genes encoding prostanoid receptors in the lamb and baboon ductus arteriosus. The ductus arteriosus was obtained from 34 lambs and eight baboons, including chronically instrumented fetuses of both species exposed to either corticosteroid or vehicle. Expression of prostanoid receptor genes was quantified using Northern blot analysis relative to each of two housekeeping genes. Expression of both the EP3 and EP4 receptor genes was detected in lamb ductus and the level of expression of both genes was unaffected by corticosteroids. Expression of the EP4 receptor gene was lower in the ductus obtained from term lambs compared with preterm lambs and was lower still in neonatal animals, whereas no variation was observed in EP3 receptor gene expression. Expression of the EP4 receptor gene was also confirmed in fetal baboon ductus arteriosus, and maternal administration of corticosteroid did not reduce EP4 receptor gene expression in the baboon. We conclude that advancing gestational age and birth may inhibit prostaglandin E2-mediated relaxation of the ductus through a corticosteroid-independent reduction in EP4 receptor gene expression.

Adrenal Cortex Hormones↗
PubMed2000

A comparison of ibuprofen and indomethacin for closure of patent ductus arteriosus.

BACKGROUND: Indomethacin is the conventional treatment for hemodynamically important patent ductus arteriosus in preterm infants. However, its use is associated with various side effects. In a prospective study, we compared ibuprofen and indomethacin with regard to efficacy and safety for the early treatment of patent ductus arteriosus in preterm infants. METHODS: We studied 148 infants (gestational age, 24 to 32 weeks) who had the respiratory distress syndrome and an echocardiographically confirmed, hemodynamically important patent ductus arteriosus. The infants were randomly assigned at five neonatal intensive care centers to receive three intravenous doses of either indomethacin (0.2 mg per kilogram of body weight, given at 12-hour intervals) or ibuprofen (a first dose of 10 mg per kilogram, followed at 24-hour intervals by two doses of 5 mq per kilogram each), starting on the third day of life. The rate of ductal closure, the need for additional treatment, side effects, complications, and the infants' clinical course were recorded. RESULTS: The rate of ductal closure was similar with the two treatments: ductal closure occurred in 49 of 74 infants given indomethacin (66 percent), and in 52 of 74 given ibuprofen (70 percent) (relative risk, 0.94; 95 percent confidence interval, 0.76 to 1.17; P=0.41). The numbers of infants who needed a second pharmacologic treatment or surgical ductal ligation did not differ significantly between the two groups. Oliguria occurred in 5 infants treated with ibuprofen and in 14 treated with indomethacin (P=0.03). There were no significant differences with respect to other side effects or complications. CONCLUSIONS: Ibuprofen therapy on the third day of life is as efficacious as indomethacin for the treatment of patent ductus arteriosus in preterm infants with the respiratory distress syndrome and is significantly less likely to induce oliguria.

Cyclooxygenase Inhibitors↗
PubMedDate not supplied

Contraction of the fetal ductus arteriosus induced by diclofenac. Case report.

The ductus arteriosus in the fetus may contract after administration of nonsteroidal anti-inflammatory drugs such as indomethacin and aspirin. We report a similar effect observed after a 36-week pregnant women was given diclofenac against flank pains. The ductus of this fetus was vasoconstricted with evidence of right ventricular hypertension. It resolved after cessation of the drug. Diclofenac is a cyclo-oxygenase inhibitor and thus carries the pharmacodynamic properties of other nonsteroidal anti-inflammatory drugs with inhibition of prostaglandin synthesis, resulting in vasoconstriction of the ductus arteriosus. We suggest monitoring of the fetal ductus state and velocities by fetal echocardiography in women treated with diclofenac.

Adult↗
PubMed1983

[Therapeutic problems with indomethacin in preterm infants with persistent ductus arteriosus].

Inhibition of PGE production in eight preterm infants with persistent ductus arteriosus and respiratory distress syndrome was associated with marked improvement in the respiratory and circulatory function in all of them. However, in six of them this effect was only transient. In the posttreatment period of five and a half days reopening of the ductus arteriosus was frequently associated with increased PGE production and a drop of indomethacin serum levels. Three of these six infants were transferred for surgical ligation and the other three infants were successfully treated with a second course of indomethacin. The margin between closure of the ductus arteriosus and the deterioration of kidney function in preterm infants treated with a presently recommended indomethacin dosage is too narrow. Before an improved therapeutic procedure has been developed indomethacin treatment for the closure of persistent ductus arteriosus should not generally be recommended in preterm infants.

Ductus Arteriosus, Patent↗
PubMed1993

The effect of gestational age and fetal indomethacin levels on the incidence of constriction of the fetal ductus arteriosus.

OBJECTIVE: To determine the effects of gestational age and fetal serum indomethacin levels on constriction of the ductus arteriosus after maternal indomethacin administration. METHODS: Twenty-five pregnant Rh-sensitized patients were given a 50-mg oral dose of indomethacin 6 hours before fetal serum indomethacin levels were determined at the time of 50 diagnostic or therapeutic funipunctures. The ductus arteriosus was evaluated with Doppler ultrasound immediately before 40 of the procedures. Constriction of the ductus arteriosus was defined as a peak diastolic flow greater than 35 cm/second. Least-squares regression and multiple regression were used for statistical analysis. RESULTS: The peak diastolic velocity of the fetal ductus arteriosus after maternal indomethacin ingestion was constant at 25 cm/second before 27 weeks, increased between 27-30 weeks to a mean of 39 cm/second, and was stable thereafter (R2 = 0.35; P < .05). There was no significant correlation between constriction of the ductus and fetal serum indomethacin levels (P = .17). CONCLUSIONS: The constrictive effect of maternal indomethacin ingestion on the fetal ductus arteriosus begins as early as 27 weeks' gestation. Constriction of the ductus arteriosus is independent of fetal serum indomethacin levels.

Blood Flow Velocity↗
PubMed1980

Management of patent ductus arteriosus in preterm babies.

There is a higher incidence of delayed closure of the patent ductus arteriosus in premature babies with respiratory distress syndrome. From July, 1975, to December, 1977, 57 small, preterm infants with patent ductus arteriosus were diagnosed at our neonatal intensive care unit. From July, 1975, until September, 1976 (first period), 23 patients were diagnosed, and 11 underwent surgical ligation of a patent ductus arteriosus. There were 3 early deaths. From October, 1976, until December, 1977, out of a total of 34 patients with diagnosed patent ductus, 18 were treated with indomethacin, and only 3 required ligation. Our present policy for patent ductus arteriosus with respiratory distress syndrome in the premature baby is to initiate early treatment with indomethacin. If this treatment fails and the infant's status deteriorates, we perform early surgical ligation of the ductus in order to minimize the time on mechanical ventilation and lessen the chances of the development of bronchopulmonary dysplasia.

Ductus Arteriosus↗
PubMed2000

Reference ranges for two-dimensional echocardiographic examination of the fetal ductus arteriosus.

OBJECTIVES: To establish reference ranges for 2D-echocardiographic examination of the fetal ductus arteriosus and its relationship to the main pulmonary artery and the aorta. METHODS: A prospective cross-sectional echocardiographic study was performed in 222 normal fetuses from 13 to 41 weeks of gestation using high resolution/color Doppler ultrasound equipment. RESULTS: Gestational age-specific reference ranges are given for the diameter of the pulmonary valve anulus, diameter of the ductus arteriosus at its beginning, middle, and end, ductal length, ductal diameter-to-pulmonary valve anulus diameter ratio, and the spatial relationship of the ductus arteriosus to the main pulmonary artery and to the aorta. CONCLUSIONS: The presented data derived from a study group of 222 normal fetuses provide in-vivo insights into the morphology of the ductus arteriosus and its relationship to the adjacent vessels. The reference ranges may be helpful in prenatal diagnosis of cardiac malformations and abnormalities of the ductus arteriosus, such as obstruction or aneurysm from 13 to 41 weeks of gestation.

Aorta, Thoracic↗
PubMed1996

Inhibitory effect of indomethacin on neonatal lung catabolism of prostaglandin E2: possible mechanism of the re-opening of the ductus arteriosus after indomethacin therapy.

Indomethacin has been used to treat patent ductus arteriosus (PDA). Re-opening of the ductus arteriosus (DA) after indomethacin therapy, however, is common, although the reason is unclear. Patency of the ductus arteriosus is thought to be maintained primarily by the vasodilatory effect of PGE2 in fetuses and neonates. The enzyme, 15-hydroxy prostaglandin dehydrogenase (15-PGDH) catalyzes the initial reactions converting the biologically active PGE2 to its inactive metabolite 15-keto-PGE2, and the lungs are a major site of this inactivation. In the present study, the effect of prenatal indomethacin treatment on the activity of neonatal rat lung 15-PGDH, and the effect of prenatal indomethacin on the re-opening of the DA induced by PGE2 were examined in rats. Indomethacin treatment at 3 mg/kg/day from day 18 to day 20 of gestation significantly decreased the activity of 15-PGDH in neonatal lungs. In a subsequent experiment, subcutaneous injection of PGE2 (4 micrograms) was given to newborn rats 3 hr after Cesarean delivery from pregnant females administered indomethacin (1, 3 mg/kg/day) as in the above experiment. The ratio of the DA to pulmonary artery was determined at intervals after injection. Maternal indomethacin treatment significantly increased the re-opening of the DA and prolonged the duration of re-opening induced by PGE2. These results suggest that the decrease in the catabolism of PGE2 in the lung is partly responsible for the failure of indomethacin therapy for PDA.

Animals↗
PubMed1993

Mechanisms of oxygen-induced contraction of ductus arteriosus isolated from the fetal rabbit.

The present study was designed to investigate the effect of O2 on intracellular Ca concentration ([Ca]i) in the ductus arteriosus and the mechanisms for O2-induced ductal contraction. The force of isometric contraction of the ring of the ductus arteriosus isolated from fetal rabbits at 30 days of gestation (term, 31 days) was measured. The ductus arteriosus was loaded with fura 2, a calcium-sensitive dye, and [Ca]i was determined from the ratio of fluorescence intensity at 340 and 380 nm excitation wavelengths. The ductus arteriosus was initially superfused with hypoxic control solutions and contraction was induced by application of oxygenated solutions. The O2-induced contraction of the ductus arteriosus was associated with increases in [Ca]i and was eliminated in the absence of extracellular calcium. An increase in [K]o from 5 to 50 mM, which causes membrane depolarization, induced ductal contraction. The calcium channel blockers verapamil, diltiazem, and nickel caused a similar inhibition of O2-induced contraction as well as KCl-induced contraction. The role of intracellular calcium stores in O2-induced ductal contraction was examined using ryanodine, an inhibitor of calcium uptake and release from the sarcoplasmic reticulum. The inhibition of O2-induced contraction by ryanodine was minimal. Infusion of glibenclamide, an inhibitor for opening the ATP-sensitive potassium channel, caused contraction of the ductus arteriosus in the hypoxic solution. Cromakalim, an opener of ATP-sensitive potassium channels, completely relaxed the contraction induced by O2. These data suggest that O2 increases [Ca]i and causes contraction in the ductus arteriosus. Application of O2 may change from anaerobic to aerobic metabolism and depolarize membrane potential by closing the ATP-sensitive potassium channel, which in turn increases calcium influx via the voltage-dependent calcium channel. Mechanisms other than the ATP-sensitive potassium channel may also be involved in the O2-induced contraction and remain to be studied.

Animals↗