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The paradoxical patent ductus arteriosus
Kathryn N. Ivey, Deepak Srivastava
Kathryn N. Ivey, Deepak Srivastava
Published November 1, 2006
Citation Information: J Clin Invest. 2006;116(11):2863-2865. https://doi.org/10.1172/JCI30349.
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Commentary

The paradoxical patent ductus arteriosus

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Abstract

The ductus arteriosus (DA) is a vessel whose patency is required for fetal survival but is incompatible with postnatal life. Because of developmental insufficiency, the DA in preterm infants often fails to close in a condition known as patent DA (PDA). Although COX inhibitors can be used to close the PDA by lowering circulating prostaglandin levels, their effectiveness is correlated with birth weight, and severely premature infants often require surgical repair. Paradoxically, targeted deletion of COX pathway components in mice results in PDA. In this issue of the JCI, Yokoyama et al. describe dual roles for prostaglandins in DA development and closure, offering new insights into the mechanism of negative effects of COX inhibitors that may influence the treatment of severely premature infants with PDA and lead to improvement of their outcomes (see the related article beginning on page 3026).

Authors

Kathryn N. Ivey, Deepak Srivastava

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Figure 1

DA during fetal-neonatal circulatory transition.

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DA during fetal-neonatal circulatory transition.
Left: During fetal deve...
Left: During fetal development, the DA shunts blood away from the lungs and directly into the systemic circulation via the aorta. Right: At birth, as PGE levels fall, SMCs in the DA constrict, bringing the intimal cushions of the DA into contact and occluding the DA lumen, so that blood flows to the neonatal lungs. This remodeling process supports the change from a fetal circulation, where blood is oxygenated in the placenta, to a neonatal circulation, where gas exchange occurs in the lungs. Blue represents oxygen-poor blood; red represents oxygen-rich blood. RA, right atrium; LA, left atrium.

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