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SUMMARY Prostaglandin-E (PGE) infusions have been used in an attempt to increase ductal patency in 11 infants aged one to 99 days with cyanotic heart disease. PGE1 was used in nine infants and PGE2 in two. Five patients had pulmonary atresia, four extreme pulmonary stenosis, one Ebstein's anomaly and one simple transposition of the great arteries. All but the oldest infant showed a satisfactory increase in oxygen saturation (average 36%) attributed to dilata-MOST DUCTUS-DEPENDENT INFANTS die in the first three months of life, many in the first few weeks. A reasonable prognosis can be offered many of these infants by reconstructive surgery, if necessary using a conduit. Such surgery is possible at any age, but the mortality in the first month is unacceptably high (B.G. Barratt-Boyes, unpublished data). Palliation with a shunt operation also incurs a relatively high mortality in the first three months of life. Of the many factors responsible for this, marked hypoxia during the operation is probably the most important. In vitro", 2 and in vivo3 4 demonstrations that E and A-type prostaglandins dilate the ductus were therefore of considerable interest, and clinical studies5'8 have shown this property to be useful in humans. We now report experience with E-type prostaglandins in 11 infants aged one to 99 days. Patients and MethodsClinical details of the 11 patients are shown in table 1. Cases 1 and 2 have been reported previously.5 Nine cases had pulmonary atresia or extreme pulmonary stenosis and were heavily or entirely dependent on ductal patency for survival. Case 8 with Ebstein's anomaly probably received most or all of his pulmonary blood flow from the ductus. Case 9 with simple transposition, who had undergone cardiac catheterization at one day of age, was thought to have little if any ductal flow at the start of the prostaglandin trial. All patients were assessed clinically with electrocardiograms and chest X-rays.All but case 8 (who was moribund at the time of initial assessment) underwent cardiac catheterization. The prostaglandin infusion was begun during cardiac catheterization in two infants and after catheterization in the remainder. PGE2 was given to cases 7 and 8, and PGEI to the remainder. An arterial cannula was inserted via the femoral or umbilical artery and an intravenous infusion was commenced. Prostaglandins were dissolved in 5% dextrose and infused at a dose of 0.1-0.75 ,g/kg/min with a Harvard constant infusion pump. Respiratory rate, pulse rate and blood pressure were recorded and any side effects were figure 1. In case 5 a preliminary trial of PGEI had been carried out when the ductus was widely patent and the arterial saturation 70%. No change occurred with this infusion. Twelve hours later the arterial saturation had fallen to 53% and the changes from this point are recorded in the figure. In all other cases the results shown are those of the first infusion. In cases 1, 2, 3 and 7 repeat in-fusions were given at a later time, the results being comparable to those shown.In nine infants im...

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