Endogenous dilator prostaglandins in congenital heart disease

Maintaining patency of the ductus arteriosus pending surgical intervention can be critical to the survival of the neonate with ductal dependent congenital heart disease. Spontaneously delayed ductal closure has been observed clinically and experimentally in newborns with critical pulmonic stenosis....

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Bibliographic Details
Published in:Pediatric cardiology 1987-01, Vol.8 (3), p.155-159
Main Authors: Hammerman, C, Aramburo, M J, Bui, K C
Format: Article
Language:English
Subjects:
6-Ketoprostaglandin F1 alpha - blood
Dinoprostone
Ductus Arteriosus, Patent - blood
Epoprostenol - biosynthesis
Heart Defects, Congenital - blood
Humans
Infant, Newborn
Oxygen - blood
Partial Pressure
Prostaglandins E - blood
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Summary:Maintaining patency of the ductus arteriosus pending surgical intervention can be critical to the survival of the neonate with ductal dependent congenital heart disease. Spontaneously delayed ductal closure has been observed clinically and experimentally in newborns with critical pulmonic stenosis. Infants with ductal dependent congenital heart lesions were therefore studied to ascertain whether there was an endogenous increase in dilator prostaglandins prolonging ductal patency. Six neonates with cyanotic lesions (group 1) and six with left ventricular obstructive lesions (group 2) were studied. Circulating PGE2 was not increased in either group. The levels of plasma 6 keto PGF1 alpha, a stable hydrolysis product of prostacyclin, were found to be elevated, but only in the cyanotic group (3143 +/- 1844 vs 404 +/- 250 pg/ml; p less than 0.05; normal less than 500 pg/ml). As expected, PaO2's were also different (36 +/- 15 vs 72 +/- 34 mmHg; p less than 0.05). It is speculated, therefore, that increased synthesis and/or release of prostacyclin, possibly mediated by the hypoxia of the cyanotic ductal dependent lesion, contributes to persistent patency of the ductus arteriosus.
ISSN:0172-0643
1432-1971
DOI:10.1007/BF02263445