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Ann Thorac Surg 1981;32:563-570
© 1981 The Society of Thoracic Surgeons
From the Division of Cardiothoracic Surgery, Children's Hospital of Philadelphia; the Department of Surgery, University of Pennsylvania School of Medicine; and the Department of Statistics of the University of Pennsylvania, Philadelphia, PA
Accepted for publication March 9, 1981.
* Address reprint requests to Dr. Stephenson, Children's Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104
Prostaglandin E1 (PGE1) is a vasodilator. Because the drug is metabolized by lung, we postulated a selective effect on pulmonary vasculature. Twenty-six patients aged 3 months to 16 years (mean, 6.5 years) were studied after repair of atrial septal defect (5), ventricular septal defect (10), tetralogy of Fallot (3), and other lesions (8). Fourteen patients also received nitroprusside. PGE1 (0.1 to 1.0 µg/kg/min) or nitroprusside (0.59 to 8.7 µg/kg/min) was infused through a central venous catheter until mean pulmonary or mean systemic arterial pressure decreased at least 10%.
Prostaglandin E1 and nitroprusside both decreased mean systemic arterial pressure and systemic vascular resistance (p < 0.05). Although both drugs caused an average decrease in pulmonary arterial pressure and resistance, nitroprusside produced a more consistent response. Side-effects limited the use of PGE1 in 5 patients. PGE1 is an effective vasodilator and has advantages for some patients, but it does not produce selective vasodilatation of pulmonary vessels.
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