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pulmonary atresia/prostaglandin
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Bladzijde 1 van 121 resultaten
[Effect of prostaglandin E1 on the hemodynamics in newborn infants with pulmonary atresia (author's transl)].
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The effect of prostaglandin E1 (PGE1) on the haemodynamics during cardiac catheterisation was studied in 6 newborn infants with pulmonary atresia and ductus-dependent pulmonary perfusion. In 4 patients with initial arterial O2-saturations between 24% and 45% pulmonary blood flow increased from a
Aneurysmal change of the ductus arteriosus after prostaglandin E1 administration for pulmonary atresia: demonstration with magnetic resonance imaging.
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We report a case of pulmonary atresia in which the ductus arteriosus underwent aneurysmal dilatation after infusion of prostaglandin E1 incorporated in lipid microspheres. To our knowledge this is the first case in which this rare morphological change has been demonstrated with the noninvasive
Ductus arteriosus dilatation by prostaglandin E1 in infants with pulmonary atresia.
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Infants with pulmonary atresia depend on patency of the ductus arteriosus for survival in the immediate postnatal period. Despite continuing hypoxemia after birth the ductus arteriosus usually constricts, thus reducing pulmonary blood flow. This often occurs while awaiting surgical palliation or
Pulmonary arterial structure in pulmonary atresia after prostaglandin E2 administration.
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Administration of long-term, oral prostaglandin E2 in two babies with pulmonary atresia did not appear to influence pulmonary arterial smooth muscle development, nor was there evidence of damage to the vessel walls, as has previously been reported after treatment of the same condition with
Prostaglandin E1 in infants with pulmonary atresia.
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Infants with pulmonary atresia are frequently dependent upon the patency of the ductus arteriosus for adequate pulmonary blood flow. Endogenous production of a dilator prostaglandin probably maintains patency of the ductus in utero. Infusion of prostaglandin E1 (PGE1) 0,1 microgram/kg/min was used
Effect of prostaglandin E1 on pulmonary circulation in pulmonary atresia. A quantitative morphometric study.
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The structural effect of prostaglandin E1 on the pulmonary circulation in pulmonary atresia has been studied by applying quantitative morphometric techniques to the injected and inflated lungs of eight babies who had received prostaglandin E1 for between 30 hours and 12 days. The most striking
Prolonged prostaglandin E1 therapy in a neonate with pulmonary atresia and ventricular septal defect and the development of antral foveolar hyperplasia and hypertrophic pyloric stenosis.
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Prostaglandin E1 (alprostadil) is widely used for maintaining the patency of ductus arteriosus in ductus-dependent congenital heart defects in neonates to improve oxygenation. Among more common side effects are fever, rash, apnoea, diarrhoea, jitteriness, and flushing. More severe side effects are
Oral prostaglandin E2 in the management of pulmonary atresia.
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Oral prostaglandin E2 in pulmonary atresia.
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Oral prostaglandin E2 in pulmonary atresia.
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[Effects of prostaglandin-E1 on patients with pulmonary atresia (author's transl)].
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Oral prostaglandin E in the management of pulmonary atresia. A case report.
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Stepwise interventional approach in a neonate with pulmonary valve atresia and intact ventricular septum.
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In neonates with pulmonary atresia and intact ventricular septum the aims of therapy are maintenance of pulmonary blood flow and right ventricular decompression in order to achieve right ventricular support of the pulmonary circulation. Recent developments in interventional heart catheterization
[Right ventricular outflow tract reconstruction in two neonates with pulmonary atresia and intact ventricular septum].
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Two neonates, aged 8 and 18 days, with pulmonary atresia and intact ventricular septum underwent right ventricular outflow tract reconstruction with an autologous pericardial transannular patch. Preoperative cardiac catheterization revealed a tripartite right ventricular morphology with
Two Extremely Low Birth Weight Infants Who Survived Functional Pulmonary Atresia with Normal Intracardiac Anatomy.
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For the first time, we report about two extremely low birth weight infants who were born at 25 and 22 weeks' gestation and who survived functional pulmonary atresia (fPA) with normal intracardiac anatomy. A slow, reflected, and bimodal blood flow pattern in the pulmonary artery (both cases) and the
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